UW Internal Medicine Flashcards
Lady has history of chest pain worse with emotional stress. No change with deep inspiration or exercise, no syncope, no SOB. Vitals, heart/ lung sounds, and EKG are all normal. Order an echo or stop testing for CAD?
Stop testing for CAD
- She’s a low-risk patient (no cardiac risk factors), so even if we did a stress test and it came back positive, it would likely be a false positive
- A transthoracic echo (TTE) would test for wall motion abnormalities during chest pain/ stress test or valvular abnormalities (like aortic stenosis) in a patient with exertional chest pain and a murmur
Old guy has problems with his central vision. Peripheral vision is good. History of cataracts, but otherwise healthy. Diagnosis?
Age-related macular degeneration (AMD)
*This is seen in patients >50 y.o.
Results from degeneration and atrophy of the central retina (macula) and surrounding structures.
**Macula= center of retina (the light-sensitive tissue that lines the inside of the eye and allows us to see in color)
Lady with stabbing pain on cheek when lightly touched, radiates from ear to jaw line. Treatment?
Carbamazepine (if this causes adverse effects: Oxcarbazepine, Baclofen, or surgical decompression of the trigeminal nerve)
This is trigeminal neuralgia (neuropathic pain along the V2/ maxillary and V3/ mandibular branches of the trigeminal nerve)
Monitor what in a patient on Carbamazepine?
Blood count
Carbamazepine can cause leukopenia (low WBC count) and aplastic anemia
What does chemosis mean?
Swelling/ edema of the conjunctiva
Normal platelet count?
150,000- 400,000
Guy traveled to Mexico. Came back with abdominal pain, vomiting, and diarrhea. These symptoms went away, but then the guy got a fever, swelling around the eyes, double vision, and splinter hemorrhages. Has eosinophilia and elevated creatine kinase. Diagnosis?
Trichinellosis (aka Trichinosis) caused by the roundworm Trichinella (“porky trickster”)
Eat undercooked pork with cysts-> gastric acid releases larvae from cysts (intestinal stage)-> female worms release new larvae a few weeks later that migrate into striated muscle (muscle stage)
- most common presentation: eosinophilia + periorbital edema + myositis (inflamed, weak muscles)
- *since the larvae migrate, patients may get systemic symptoms like fever and splinter hemorrhages
Dengue fever usually presents with pain where?
Behind the eye (retro-orbital pain)
Why might shistocytes/ helmet cells show up on blood smear in a patient with a replaced heart valve?
Prosthetic heart valves can destroy RBCs that cross the valve-> schistocytes/ helmet cells (fragmented RBCs)
Is haptoglobin increased or decreased in hemolytic anemia?
Decreased
Haptoglobin binds up free hemoglobin (Hb). In hemolytic anemia, there’s a lot of broken up RBCs, so there’s a lot of free Hb for haptoglobin to pick up. Since haptoglobin is getting used up, it is decreased.
Meaning of conjunctival pallor?
Pale conjunctiva
Patient has macrocytic anemia, shiny tongue, SOB on exertion, and depigmented areas over the arm suggestive of vitiligo. Cause of the anemia?
Pernicious anemia (antibodies against intrinsic factor)-> vitamin B12 deficiency
*Macrocytic= B12 or folate deficiency. Glossitis is seen in both these, since these deficiencies impair DNA synthesis (and therefore impair epithelial replication). Folate deficiency is usually seen in alcoholics or malnourished. Having vitiligo makes pernicious anemia more likely- if you have 1 autoimmune dz you’re at greater risk for another since your immune system sucks
Patient went to the Caribbean and came back with fever, malaise, rash, lymphadenopathy, and polyarthralgias (pain in joints). Diagnosis?
Chikungunya fever
- caused by the Aedes mosquito in the Caribbean
- supportive treatment
Patient has aortic dissection (tearing chest pain) + orthopnea (SOB when lying down) to the point that he refuses to lay down. Most likely cause of the SOB?
Aortic regurg
-Aortic dissection can lead to aortic regurg if blood from the intimal tear extends to the aortic valve
-This can cause 4 symptoms:
1. Hypotension (blood is regurging backwards, so less blood is being pumped forwards)
2. Sudden onset worsening chest pain
3. Pulmonary edema
4. Orthopnea (SOB lying down)
(2-4 are due to: blood from aorta-> LV and backing up into lungs)
**aortic dissection can also cause cardiac tamponade (if blood from the intimal tear enters into the pericardium and restricts filling of the heart). This would NOT cause pulmonary edema.
Patient just took Bactrim for a UTI. She is on Phenytoin for seizures. Recently, she has had an unsteady gait and nystagmus. What’s going on?
Phenytoin toxicity (ataxia and nystagmus are side effects of Phenytoin)
-Bactrim (TMP-SMX)= P450 inhibitor, so it blocks P450 metabolism in the liver—> drug stays in body longer. Phenytoin working in the body longer—> toxicity.
40 y.o. Lady from India has episodes of upper abdominal pain and burning that waxes and wanes. Feels bloated after meals. Positive stool guaiac (occult blood in stool). Most likely diagnosis?
H. Pylori
*dyspepsia (indigestion/ heartburn) can be—> from NSAIDs, GERD, H Pylori, etc.
GERD wouldn’t cause blood in stool. Since she has blood in stool and from India (low-income), H. Pylori is most likely.
**diagnose with urea breath test or stool antigen test. Endoscopy is reserved for patients >55 y.o. Or those with alarm symptoms (weight loss, bleeding, anemia, dysphasia, persistent vomiting).
What is dyspepsia?
Indigestion/ heartburn
What is bradyarrhythimia?
Bradycardia <60 bpm
TIA vs. stroke?
TIA (transient ischemic attack or “mini stroke”)- blockage is temporary and blood flow returns on its own. Stroke symptoms go away on their own
Stroke- “brain attack” where blockage is permanent
Lady with a hx of MS and hyperlipidemia has speech arrest and right arm weakness for <30 minutes. What are 2 meds we should give her?
Aspirin (ASA) and a statin
Why? She had a TIA (classic stroke symptoms for <24 hrs that resolved on their own). The treatment for TIA is to address the risk factors- so give aspirin (to prevent platelet aggregation and stroke) and give a statin (to lower her cholesterol).
**This presentation is NOT an MS exacerbation (MS attacks last for days or weeks). If it were, we could treat the flare up with glucocorticoids, immunoglobulins, or plasma exchange therapy (since MS is an autoimmune condition and we want to decrease the immune system’s damage).
Women has burning upper abdominal pain, constipation, and blood in stool. Calcium is high, phosphorus is low. What syndrome does she likely have?
MEN 1 (multiple endocrine neoplasia type 1)= “pans of pitted pears” -pancreatic, pituitary, and parathyroid tumors
- Has a pancreatic tumor (ZE syndrome)—> burning upper abdominal pain and GI bleed (tumor can invade into duodenum).
- Has a parathyroid tumor—> release PTH (primary hyperparathyroidism), which increases calcium absorption and phosphorus wasting.
- That’s 2/3, so MEN 1 is likely and we would want to check for a pituitary tumor also.
Sarcoidosis effect on calcium levels?
Can cause hypERcalcemia
Due to increased conversion to 1,25 active vitamin D—> more calcium and phosphorous reabsorption
What is Milk-alkali syndrome?
Hypercalcemia + metabolic alkalosis + AKI due to taking too much calcium (can be from taking too many Tums pills…since Tums= calcium carbonate)
**too much calcium has multiple effects on the kidneys and ultimately causes diuresis and stimulates bicarb reabsorption-> met alkalosis
What is a plantar reflex?
Babinski
Old guy with memory loss and muscle spasms when startled. He also has nystagmus, hypokinesia, and positive Babinski (plantar reflex). EEG shows periodic sharp-wave complexes. Diagnosis?
Creutzfeldt-Jakob disease (CJD)
- prion disease (usually sporadic, but can be due to contaminated corneal transplants).
- key findings: startle response and sharp waves on EEG
- *as it progresses, patients may lose ability to move and speak (txt is supportive)
Lady has temporal (giant cell) arteritis and gets treated. 6 months later her muscles are weak and she has trouble going up stairs or standing from a chair. Most likely cause?
Drug-induced myopathy
-glucocorticoids (used to treat giant cell arteritis) can cause myopathy (think of Cushing’s secondary to too much glucocorticoid use…skin thinning, fat redistribution, and muscle thinning!)
What are the pneumonia vaccine guidelines for seniors 65+?
One 13-valent pneumococcal conjugate vaccine (PCV13) +
One 23-valent pneumococcal polysaccharide vaccine (PPSV23) at least 6-12 months later
*give add’l PCV13 and PPSV23 vaccines to high-risk patients (CSF leaks, sickle cell, cochlear implants, asplenia/ immunocompromised)
**give one PPSV23 before age 65 too for some patients (smokers or chronic medical problems like heart/ lung/ liver dz or DM)
What’s a normal pupil size?
2-4 mm in light
How would Phenytoin toxicity present?
Nystagmus, ataxia, confusion
Decreased sensation over 4th and 5th digits and weak grip. What nerve is probably damaged and where?
Ulnar nerve
At the elbow (medial epicondylar groove)
*ulnar nerve syndrome can be caused by prolonged compression on the ulnar nerve from leaning on the elbows while working at your desk
Incidence vs. prevalence?
Incidence= # new cases
Prevalence= total cases
If a man abuses steroids (testosterone), will his levels of GnRH, LH, and FSH be high or low?
All low
-the exogenous testosterone will feedback and inhibit GnRH, LH, and FSH production (-> low endogenous testosterone, small testes, possible infertility)
After treatment with Dapsone, a patient developed fatigue and dark urine. Why?
G6PD deficiency
- in this condition, RBCs can’t make enough NADPH to protect against oxidative injury. Some meds (Dapsone, TMP/SMX, Primaquine), foods (Fava beans), and infections cause oxidative damage and bring on anemia attacks in patients with this
- *hemolytic anemia-> blood in urine (dark urine)
What type of drug is Enoxaparin?
Low-molecular weight heparin (LMWH)
Patient has a DVT. Is treated with Enoxaparin (LMWH). Platelet count goes down. Why?
This is heparin-induced thrombocytopenia (HIT)
- bad reaction to heparin where heparin binds to platelet factor 4 (PF4) and antibodies form against the hep-PF4 complex. These antibodies attack platelets—> thrombocytopenia (low platelets) and stick them together—> clotting (opposite of what you’d expect when giving an anti-coagulant).
- discontinue the hep immediately and pick another anticoagulant to treat with!
Reg chest X-rays, what does “bilateral basilar lucency” mean?
Lucency= shows up dark on x-ray
-means it’s less dense (like air-filled lungs in emphysema)—> more X-rays pass through
Basilar= bottom of lungs (opposite of apex, which is the pointy top of the lungs)
So…”bilateral basilar lucency” means the bottom of both lungs appears darker (air-filled) on X-ray
38 y.o. man with SOB and cough, worse on exertion. Smoked 2 years, otherwise no medical hx. Breath sounds are decreased on the bottom of both lungs. Diagnosis?
Alpha-1 antitrypsin deficiency—> panacinar emphysema (destruction of lower lobes *vs. emphysema due to smoking alone would be centriacinar and cause destruction of upper lobes “smoke rises”)
How do you diagnose Alpha-1 antitrypsin (AAT) deficiency (besides going off the history and physical)?
Measure serum AAT levels (should get pulmonary function tests too)
What is nephrolithiasis?
Kidney stones
Alcoholic is having seizures. Cr is 2.4. RBCs are found in his urine. Diagnosis?
Rhabdomyolysis
*seizures-> skeletal muscles overexertion-> release of myoglobin into the blood-> clogs up renal tubules and causes renal injury
Normal Cr? Normal BUN? Normal BUN:Cr ratio?
Cr- 0.6-1.2
BUN- 7-25
BUN/CR- around 15
Normal calcium levels?
8.5-10ish
Normal potassium (K+) level?
3.5-5.0
Normal Na+ level?
135-145
Paraneoplastic syndromes in small cell lung CA (4) vs. squamous cell lung CA (1)?
Small cell:
- SIADH
- Lambert-Eaton
- ACTH (Cushing’s)
- Anti-Hu antibodies
Squamous cell:
1. PTHrP (-> hypercalcemia)
Former smoker has a lung mass and calcium level of 14.5. Why is calcium at this level?
Calcium is high (normal would be 8.5-10ish…14 is very high)
This is due to squamous cell carcinoma of the lung-> PTHrP (paraneoplastic syndrome)-> excess calcium reabsorption (and phosphorous wasting)
-This is also known as “hypercalcemia of malignancy”
How do we treat hypercalcemia in the short-term? Long-term?
Short term: Give normal saline (and calcitonin)
- why? Hypercalcemia-induced DI (high calcium interferes with renal channels that allow ADH to work to retain water)-> hypercalcemia patients pee a lot and are volume depleted, so you have to restore volume/ hydrate
- may also give Calcitonin (directly blocks osteoC’s from breaking down bone and releasing calcium-> so, they lower calcium levels in the blood)
- *don’t give loop diuretics (even though they can lower calcium levels) unless they have HF (not worth the side effect of worsening volume depletion)
Long term: Give bisphosphonates
*why? Bisphosphonates stimulate apoptosis of osteoClasts (they stop osteoC’s from breaking down bone and releasing calcium-> so, they lower calcium levels in the blood)
Normal platelet count?
150,000- 400,000
Normal Hb in male? Female?
Normal Hb in males= 13.5- 17.5
Normal Hb in females= 12-16
a little lower due to bleeding once a month/ menstrual cycles
Treatment for botulism?
Horse-derived (equine) antitoxin therapy
Treatment for Guillain-Barre?
Plasmaphoresis (therapeutic plasma exchange)
*GB occurs when the immune system attacks nerves (can be after Campylobacter or a flu shot…)
What is antiphospholipid antibody syndrome?
The presence of antiphospholipid antibodies + you have blood clots (DVT, PE, stroke, or MI) or pregnancy problems (miscarriages or premature birth from placental insufficiency or preeclampsia)
**Antiphospholipid antibodies are seen in SLE (lupus) (though not specific to it). They can cause 3 problems: (1) antiphospholipid antibody syndrome, (2) increased PTT, (3) false positive syphilis test (RPR/ VDRL)
What is spontaneous bacterial peritonitis (SBP)?
A bacterial infection of the ascitic fluid of the peritoneum
(So, it’s when a patient has ascites, usually secondary to cirrhosis, and that fluid gets infected)
Man with hx of cirrhosis secondary to chronic hep C presented with confusion. He was found to have hepatic encephalopathy and spontaneous bacterial peritonitis (infection of ascitic fluid). He was given Lactulose and Cefotaximine. Since admission and all of this, his Creatinine has gone up. Most likely cause?
Hepatorenal syndrome
Most likely diagnosis in a Mississippi patient who was initially thought to have sarcoidosis (cough, hilar lymphadenopathy, erythema nodosum, and non-caseating granulomas)?
Histoplasmosis
*Blasto is also seen in the Mississippi region, but usually does not involve hilar lymphadenopathy
Where are these fungi found?
- Histoplasmosis
- Blastomycoses
- Coccidioides
- Paracoccidioides
- Histoplasmosis- Mississippi/ Ohio river valley (Midwest)
- Blastomycoses- Great Lakes/ Ohio river valley (Midwest)
- Coccidioides- Southern US (Cali, Arizona, northern Mexico)
- Paracoccidioides- South America, Brazil
Guy has a hx of IV drug abuse, endocarditis, and stroke (made him wheelchair-bound). Presents with right calf pain and swelling. On physical exam, there is hepatosplenomegaly. Abdomen is distended with shifting dullness suggestive of ascites. Most likely cause of the ascites?
Chronic liver disease
- IV drug use= high-risk for hep C w/ chronic liver dz (cirrhosis)—> ascites (the portal HTN causes fluid to accumulate in the peritoneum)
- IV drug use also—> endocarditis with embolic stroke. Stasis (wheelchair-bound) following the stroke—> DVT. But DON’T be distracted by everything going on w/ this patient! The question is just asking why does he have ascites? 80% of ascites is due to liver failure and you can trace this to his IV drug abuse.
Man with hx of IV drug abuse has dark urine and jaundice. Total bilirubin, direct (conjugated) bilirubin, alk phos, and AST are all high. Abdomen is not tender. Next best step to diagnose?
Ultrasound the abdomen
(High serum alk phos suggests cholestasis/ reduced bile flow, possibly due to an obstruction/ stone. U/S will help you look for intrahepatic or extrahepatic causes of biliary obstruction.)
50 year old lady with hx of GERD. Has episodes of hands turning bluish in the cold. Her hands are puffy and lungs have crackles. Diagnosis? Associated with what 2 antibodies?
Systemic sclerosis (diffuse type)
- anti-Scl-70 antibody (aka anti-DNA topoisomerase-1 antibody)
- anti-RNA polymerase III
*Systemic sclerosis= autoimmunity + non inflammatory vasculopathy + collagen deposition w/ fibrosis.
2 sub-types: (1) diffuse (involves the skin all over and early visceral involvement- interstitial lung dz), (2) limited aka CREST syndrome (face and fingers)
**CREST= Calcinosis (calcium deposits) and anti-Centromere antibody
Raynaud’ s phenomenon
Esophageal dysmotility (GERD0
Sclerodactyly (thickened skin on hands and feet)
Telangiectasia (dilated blood vessels)
What does CREST syndrome stand for?
Calcinosis (calcium deposits) and anti-Centromere antibody
Raynaud’ s phenomenon
Esophageal dysmotility (GERD0
Sclerodactyly (thickened skin on hands and feet)
Telangiectasia (dilated blood vessels)
What is the drug Memantine used for?
Severe Alzheimer’s disease
- it blocks NMDA glutamate receptors
- may improve cognitive symptoms
Lady just flew home from Central Asia. Has SOB, chest pain, and hemoptysis. HR is 106, RR is 28. Most likely diagnosis?
Pulmonary embolism (PE)
- She was on a long flight, has SOB, and is coughing up blood. Red flags!
- typical PE presentation= tachypnea (rapid breathing) and tachycardia in addition to SOB. This is because she has the pulm artery occluded-> dec oxygenation-> heart tries to compensate.
Patient is anxious, confused, has conjunctival injection. What substance?
Marijuana
(Conjunctival injection= bloodshot eyes)
*increases appetite, HR, breathing, causes dry mouth, and bloodshot eyes. Also slows reaction time-> car accidents.
What acid-base disturbance can AKI cause?
Non-nation gap metabolic acidosis
-from retention of uremia and impaired acid excretion (if you can’t pee out the acid, it accumulates in the blood)
Why might hypoventilation cause fatigue?
Breathing less= less oxygen being delivered to organs in the body to provide energy
In nephrogenic DI (like due to lithium), will sodium levels go up or down? Will blood or urine have a higher osmolarity?
Nephrogenic DI (not responding to ADH)-> not retaining water-> pee more-> [Na+] will go up-> HYPERNATREMIA (high Na+)
Blood will be more concentrated (HIGHER OSMOLARITY) than the urine (urine is more dilute since you’re peeing more)
How can sodium levels differentiate nephrogenic DI vs. psychogenic polydipsia?
Nephrogenic DI (not responding to ADH)-> not retaining water-> pee more-> [Na+] will go up-> HYPERNATREMIA (high Na+)
Psychogenic polydipsia (drinking water like a crazy person)-> you’re putting so much water into the body that it dilutes [Na+]-> HYPONATREMIA (low Na+)
What is the DASH diet?
DASH= Dietary Approaches to Stop Hypertension
-this is the diet you put HTN patients on
(Involves eating fruits, veggies, whole grains, low-fat, low salt, high potassium foods)
What is UP/Cr?
Urine protein over creatinine ratio
A way to estimate how much protein is being spilled in the urine per day
What is ankle-brachial index?
Ratio of BP at the ankle to BP in the upper arm (brachial)
- If BP in the ankle is lower than in the arm, it suggests blocked arteries in the ankle due to peripheral vascular disease (PAD)
- used to check when patient has claudication, dermal atrophy, and absent distal pulses
A patient had a previous MI complicated by LV systolic dysfunction (the heart isn’t pumping so well anymore-> ejection fraction <30%). What deadly condition is this patient at risk of?
Sudden cardiac death (SCD) due to ventricular arrhythmia
Guy is brought in by his GF for confusion. He moved into a mobile home yesterday and had headache, nausea, and dizziness. This morning she went over to check on him and found him confused in bed in his urine. What test will most likely diagnose him?
Measuring carboxyhemoglobin level
*this is likely carbon monoxide (CO) poisoning from an old heater. Hb binds CO instead of oxygen (CO has a greater affinity)—> carboxyhemoglobin. Less oxygen delivered to tissues (left shift).
What is Well’s criteria?
A calculator to assess the probability a patient has a PE (pulmonary embolism)
*if total score (based on clinical signs of DVT, previous DVT/ PE, tachycardia, recent surgery, hemoptysis/ cancer) is >4, a PE is likely
If PE is on your differential but is unlikely (based on Wells criteria), what test can you do to rule it out completely?
Check the D-dimer (make sure it’s less than 500)
- D-dimer is sensitive, but not specific for PE. So, you get this to make sure you can rule out PE.
- *If PE is likely (based on Wells criteria), don’t get a D-dimer…go straight to CT pulmonary angiogram (aka spiral CT) (or V/Q scan if you can’t do the pulmonary angiogram bc the patient has bad kidneys and can’t handle the contrast) to diagnose.
If PE is on your differential and is LIKELY (based on Wells criteria), what test do you do?
Get a CT pulmonary angiogram (aka spiral CT) to diagnose
Unless your patient has kidney problems (in which case they can’t handle the IV contrast needed to do the pulmonary angiogram)—> then get a V/W scan to diagnose
What number is an elevated D-dimer?
> 500
What antibiotic can you give as empiric treatment of traveler’s diarrhea (ETEC)?
Ciprofloxacin (short-course)
*if symptoms fail to improve, test for something else (ex: may be parasitic like Giardia and require Metronidazole)
35 year old guy with PMH of Bipolar (on Risperidone) comes in for fatigue, headache, and decreased libido. Testosterone- low TSH- low T4- low Prolactin- high Most likely diagnosis?
Pituitary adenoma
- anterior pituitary—> FLAT PiG (FSH, LH, ACTH, TSH, Prolactin, GnRH)
- mass effect—> headache and visual disturbance. Production of most hormones will be decreased due to compression of normal pituitary cells. But, prolactin is high due to anatomic disruption of the dopamine brake onto prolactin.
- *NOT Hashimotos/ hypothyroidism bc T4 would be low, but TSH would be high due to negative feedback.
- *NOT Risperidone side effect bc that’s an anti-dopamine drug-> takes brake off prolactin-> high prolactin, but does not affect these other hormones.
What valvular problem is common in ankylosing spondylitis?
Aortic regurg
*Ankylosing spondylitis= a seronegative spondyloarthritis (FA pg 461- lack of Rheumatoid factor, axial skeleton involvement, HLA-B27) with spinal fusion—> bamboo spine. Patients can also get uveitis and aortic regurg (aortic inflammation-> aortic aneurysm-> pulls on valve-> regurg).
**These patients are at risk for vertebral fractures with minimal trauma! (Increased osteoclast activity in the setting of chronic inflammation)
A patient has a MI of the LAD. 4 days later, she is hypotensive with tachycardia. There are crackles over her lungs and her extremities are cold. EKG shows deep T wave inversion in leads V1-V5. Most likely cause of her deterioration?
Interventricular septum rupture (complication 3-5 days post-MI)
-> cardiogenic shock (hypotension, pulm edema, confusion due to poor pumping and poor organ perfusion). Cold extremities due to shunting of blood to core vital organs.
Male patient undergoing chemo for Seminoma comes to the ED for fever and chills, nothing else going on. He has mucosal pallor (pale skin), low Hb and Hct, and low leukocytes and neutrophils. Diagnosis and treatment?
Febrile neutropenia (fever + low neutrophils, specifically absolute neutrophil count <1500)
Treat with an anti-pseudomonas beta-lactam agent (these bugs are often responsible)—
Cefepime (4th gen cephalosporin), Meropenem (carbapenem), or Piperacillin-Tazobactam (extended-spectrum penicillin)
*Chemo patients are at higher risk for this and you need to give emergent empiric antibiotics to prevent progression to sepsis!
Patient with PMH of Genital herpes comes in with scaley rashes looking like psoriasis. What screening test should you offer him?
HIV test
*HIV is associated with flares of psoriasis. Other things that can worsen psoriasis— skin trauma, withdrawal from glucocorticoids, and certain meds (anti-malaria, indomethacin, propranolol)
AIDS patients are at greatest risk for a CMV (cytomegalovirus) infection with a CD4 count less than what?
CD4 < 50
“Charity drive 50 cents”
Treatment for CMV esophagitis (AIDS patient with CD4 <50 with linear ulcerations)?
Ganciclovir
*Herpes Simplex esophagitis (well-circumscribed, round ulcers as opposed to linear ulcers in CMV) is treated with Acyclovir
HIV patient has a CD4 count of 300. She has a lobular pneumonia, diagnosed by symptoms and chest X-ray. What is the most likely organism responsible for the pneumonia?
Strep pneumo
*Don’t assume it’s PCP pneumonia just bc she has HIV! That is seen in HIV patients with CD4 <200. Still, step pneumo is the no. 1 cause of lobular CAP!
AIDS patient with CD4 <50 and bloody diarrhea. Most likely cause?
Cytomegalovirus (CMV colitis)
- common causes of diarrhea in HIV patients:
1) Cryptosporidium—CD4 <180 (severe watery diarrhea, low-grade fever)
2) Microsporidium—CD4 <100 (crampy watery diarrhea, usually no fever)
3) MAC—CD4 <100 (watery diarrhea and high fever)
4) CMV—CD4 <50 (bloody diarrhea, abdominal pain, low-grade fever)
HIV patient has had a cough for 2 months, no hemoptysis. Was hospitalized 6 months ago for seizures. CXR shows cavitation in the right upper lobe. Most likely diagnosis?
Reactivation TB (affects upper lobes)
- not likely to be aspiration pneumonia bc that is found in lower lobes (due to gravity)
- you do not HAVE TO HAVE hemoptysis for it to be TB!!! Also, note this guy’s HIV status puts him at increased risk for TB
What the heck is Strep Sanguinus?
It’s in the family of Step Viridans
*think of it when there is a patient with a heart problem who gets a dental procedure done!
Lady has painful swelling of the left face. There is a raised red rash with sharply-demarcated borders including the left ear. She also have fever + chills. What bug is responsible?
Group A strep (Strep Pyogenes)
This is Erysipelas (superficial skin infection of the upper dermis *like cellulitis but more superficial)
When is Toxoplasma prophylaxis indicated?
In HIV patients with CD4 <100
When is CMV prophylaxis indicated?
In some organ transplant recipients
HIV patient not taking his meds. Has had weight loss, fever, night sweats, cough, and SOB for 3 weeks. There are small ulcers on his hard palate, enlarged lymph nodes, and lung crackles. What test should you order?
Urine Histoplasma antigen
(This sounds like disseminated histoplasmosis)
*treat with Amp B
What is the most appropriate empiric antibiotic to start an endocarditis patient on with a hx of IV drug abuse?
Vancomycin
-it is broad spectrum and has MRSA coverage
Wisconsin guy has fever, night sweats, productive cough, and weight loss. Also has crusty skin lesions, lytic lesions on ribs, and consolidation on his left upper lung. Diagnosis?
Blastomycosis
*seen in the Mississippi/ Ohio river valley (Wisconsin has the highest infection rate)
Teenager has episodes of “chest fluttering.” BP is normal, but pulse is 210. EKG shows narrow complex tachycardia. What diagnosis should be on the differential?
Wolff-Parkinson-White syndrome
-going through an accessory “secret pathway” (bundle of Kent) that bypasses the rate-slowing AV node-> ventricles get depolarized before they should (shows up on EKG as delta waves).
What is long QT syndrome?
When you have a long QT interval (QT= ventricular depolarization + depolarization, so the entire systole)
- > 450 mace in males or >470 mace in females
- can be congenital or acquired
- risk for sudden cardiac death (due to Torsades or polymorphic ventricular tachycardia)
What is micturition?
Urination
What is an electrocardiogram?
ECG! (Same thing as EKG)
Old guy felt like he was going to pass out while running. He had a similar episode before. You did a physical exam, significant for a systolic ejection murmur at the right 2nd intercostal space. You order an EKG, which showed LV hypertrophy. Next step?
Order an echocardiogram
This guy most likely has aortic stenosis (exertional syncope, systolic murmur, LV hypertrophy). Get an echo any time you suspect a structural/ valvular heart disease (aortic stenosis, HOCM, LV dysfunction, cardiac tamponade, etc.)
*do NOT stress test symptomatic severe aortic stenosis
20 year old lady with episodes of sharp chest pain for 3 weeks. Has systolic murmur at the apex that shortens with squatting. Diagnosis?
Mitral valve prolapse
*Apex= mitral region
Systolic murmur= MVP or mitral regurg
Squatting= increased preload (kink veins in legs-> more ‘milking’ of blood to heart)
Murmur is softer with squatting= MVP (more preload helps the valve to be more crisp as opposed to floppy where it doesn’t align well)
**Do an echo to confirm the diagnosis. Symptoms are benign.
Guy comes in with sudden onset palpitations. He is found to be in a-fib. BP is 112/70 and O2 sat is 92. He is full code.
He suddenly becomes unresponsive. Cardiac monitor still shows a-fib, but there’s no palpable pulse and he has agonal breathing (gasping). What do you do next?
Chest compressions
- The heart has an abnormal rhythm going on, but it is not effectively pumping blood out to the extremities, so you can’t feel a pulse (this is called pulseless electrical activity).
- ACLS guidelines say do CPR and give epi (beta>alpha agonist, so helps improve contractility and is a vasopressor-> vasoconstricts to improve cerebral and coronary perfusion).
*Although we should cardiovert new a-fib patients (had it <48 hrs) or a-fib patients who are unstable, if they are so unstable they go into a non-perfusing rhythm, you follow ACLS guidelines!
Asystole vs. Pulseless electrical activity (PEA)?
Asystole- Cardiac arrest
No electrical activity
Monitor is flat-lined
Pulseless electrical activity (PEA)- A non-perfusing rhythm
There is an abnormal heart rhythm (ex: a-fib), but the heart isn’t effectively pumping blood out, so there’s no palpable pulse (or measurable BP)
Monitor shows the abnormal rhythm
**NOTE: 3 rhythms cannot be PEA: (1) V-fib, (2) V-tach, (3) Asystole. Why? Bc we don’t expect a pulse with these rhythms. PEA is an organized electrical activity where we expect to see a pulse but we don’t have one.
What does ACLS stand for? What does CPR stand for?
ACLS= Advanced Cardiac Life Support
(guidelines on what to do if a patient is in cardiac arrest)
CPR= Cardiopulmonary Resuscitation
What are the reversible causes of asystole/ pulseless electrical activity? “5 H’s and 5 T’s”
(You want to consider these when doing chest compressions and giving epi…if you figure out the source of the problem, you may be able to correct the heart’s rhythm and save the patient’s life!)
Hypovolemia Hypoxia Hydrogen ions (acidosis) HypOkalemia/ HyPERkalemia Hypothermia
Tension pneumothorax Tamponade, cardiac Toxins (narcotics, benzos) Thrombosis (pulmonary or coronary) Trauma
Can you shock a patient in Asystole?
NO
Asystole= they are flat-lined. There is ZERO electrical activity in the heart, so shocking them will not work (shocks work by feeding off of electrical activity). Do chest compressions, give epi (every 3-5 min), and try to figure out why the patient went into asystole bc there may be a reversible cause.
2 shockable rhythms? 2 non-shockable rhythms?
SHOCK:
- V-fib (ventricular fibrillation)
- V-tach (ventricular tachycardia)
* *note: Torsades is a subcategory of ventricular tachycardia- shock it.
NON-SHOCKABLE:
- Asystole
- Pulseless electrical activity (PEA)
Rap song: “Defib for V-fib and pulseless V-tach. Don’t defib asystole, you won’t get them back!”
Define orthostatic hypotension.
Decrease in BP by 20 systolic or 10 diastolic when standing
*may be accompanied by an increase in HR
Why are old people more likely to get orthostatic hypotension (big drop in BP when they stand, making them momentarily lightheaded)?
Aging-> some baroreceptor activity is lost
*normally: you stand-> gravity is working against you so vessels have to constrict in the lower extremities to ‘milk’ blood up to the heart so it can pump enough to maintain BP. For the moment that BP is dropped right when you stand, baroreceptors (on carotid sinus) respond to decreased stretch-> decrease firing-> this increases sympathetic stimulation to raise the BP to baseline.
Young man faints when exercising. Has a crescendo-decrescendo systolic murmur in the left sternal border. Diagnosis?
HOCM
Basically a functional aortic stenosis, since the intraventricular septum is in the way of aortic outflow
IV drug user had an episode of syncope. Has a diastolic murmur at the left sternal border. Platelet count is elevated and EKG shows 2nd degree AV block. Diagnosis?
Perivalvular abscess
*Be suspicious of perivalvular abscess anytime a patient has endocarditis + conduction abnormalities on EKG (the abscess can extend into the conduction pathway, messing it up). Endocarditis alone wouldn’t cause AV block or syncope.
Man comes in for palpitations and SOB on exertion. He recently binge drank. HR is 130. EKG shows no clear P waves. Echo shows EF=35%, mitral regurg, and dilated LA and LV with global hypokinesis. What’s going on?
Alcohol-> A-fib w/ RVR (rapid ventricular response)-> tachycardia-mediated cardiomyopathy (the prolonged arrhythmia and rapid ventricular rate is causing HF)
*treat with aggressive rate and rhythm control
**note: the mitral regurg in this patient is just due to the fact that the ventricles are overloaded
What is tachycardia-mediated cardiomyopathy? How do you treat it?
When you have a tachyarrhythmia (heart is beating super fast, out of rhythm for a while) that leads to HF
(*can be due to a-fib, a-flutter, v-tach, etc.)
Treat with aggressive rate or rhythm control
(*AV nodal blocking agents, antiarrhtymic drugs, ablation of arrhythmia, etc.)
37 year old lady who immigrated from Cambodia presents with stroke symptoms. Over the past several months, she has had palpitations, SOB on exertion, and hemoptysis. Most likely explanation?
Rheumatic heart disease-> mitral stenosis-> a-fib-> stroke
*remember that mitral stenosis (MS) over time-> increased LA pressure. This predisposes to a-fib. This also leads to pulmonary vascular congestion, explaining the hemoptysis.
What is “flash pulmonary edema?”
Acute pulmonary edema secondary to increased cardiac filling pressures (such as after an MI)
What is micturition?
Urination
What is an electrocardiogram?
ECG! (Same thing as EKG)
Old guy felt like he was going to pass out while running. He had a similar episode before. You did a physical exam, significant for a systolic ejection murmur at the right 2nd intercostal space. You order an EKG, which showed LV hypertrophy. Next step?
Order an echocardiogram
This guy most likely has aortic stenosis (exertional syncope, systolic murmur, LV hypertrophy). Get an echo any time you suspect a structural/ valvular heart disease (aortic stenosis, HOCM, LV dysfunction, cardiac tamponade, etc.)
*do NOT stress test symptomatic severe aortic stenosis
20 year old lady with episodes of sharp chest pain for 3 weeks. Has systolic murmur at the apex that shortens with squatting. Diagnosis?
Mitral valve prolapse
*Apex= mitral region
Systolic murmur= MVP or mitral regurg
Squatting= increased preload (kink veins in legs-> more ‘milking’ of blood to heart)
Murmur is softer with squatting= MVP (more preload helps the valve to be more crisp as opposed to floppy where it doesn’t align well)
**Do an echo to confirm the diagnosis. Symptoms are benign.
Guy comes in with sudden onset palpitations. He is found to be in a-fib. BP is 112/70 and O2 sat is 92. He is full code.
He suddenly becomes unresponsive. Cardiac monitor still shows a-fib, but there’s no palpable pulse and he has agonal breathing (gasping). What do you do next?
Chest compressions
- The heart has an abnormal rhythm going on, but it is not effectively pumping blood out to the extremities, so you can’t feel a pulse (this is called pulseless electrical activity).
- ACLS guidelines say do CPR and give epi (beta>alpha agonist, so helps improve contractility and is a vasopressor-> vasoconstricts to improve cerebral and coronary perfusion).
*Although we should cardiovert new a-fib patients (had it <48 hrs) or a-fib patients who are unstable, if they are so unstable they go into a non-perfusing rhythm, you follow ACLS guidelines!
Asystole vs. Pulseless electrical activity (PEA)?
Asystole- Cardiac arrest
No electrical activity
Monitor is flat-lined
Pulseless electrical activity (PEA)- A non-perfusing rhythm
There is an abnormal heart rhythm (ex: a-fib), but the heart isn’t effectively pumping blood out, so there’s no palpable pulse (or measurable BP)
Monitor shows the abnormal rhythm
**NOTE: 3 rhythms cannot be PEA: (1) V-fib, (2) V-tach, (3) Asystole. Why? Bc we don’t expect a pulse with these rhythms. PEA is an organized electrical activity where we expect to see a pulse but we don’t have one.
What does ACLS stand for? What does CPR stand for?
ACLS= Advanced Cardiac Life Support
(guidelines on what to do if a patient is in cardiac arrest)
CPR= Cardiopulmonary Resuscitation
What are the reversible causes of asystole/ pulseless electrical activity? “5 H’s and 5 T’s”
(You want to consider these when doing chest compressions and giving epi…if you figure out the source of the problem, you may be able to correct the heart’s rhythm and save the patient’s life!)
Hypovolemia Hypoxia Hydrogen ions (acidosis) HypOkalemia/ HyPERkalemia Hypothermia
Tension pneumothorax Tamponade, cardiac Toxins (narcotics, benzos) Thrombosis (pulmonary or coronary) Trauma
Can you shock a patient in Asystole?
NO
Asystole= they are flat-lined. There is ZERO electrical activity in the heart, so shocking them will not work (shocks work by feeding off of electrical activity). Do chest compressions, give epi (every 3-5 min), and try to figure out why the patient went into asystole bc there may be a reversible cause.
2 shockable rhythms? 2 non-shockable rhythms?
SHOCK:
- V-fib (ventricular fibrillation)
- V-tach (ventricular tachycardia)
* *note: Torsades is a subcategory of ventricular tachycardia- shock it.
NON-SHOCKABLE:
- Asystole
- Pulseless electrical activity (PEA)
Rap song: “Defib for V-fib and pulseless V-tach. Don’t defib asystole, you won’t get them back!”
Define orthostatic hypotension.
Decrease in BP by 20 systolic or 10 diastolic when standing
*may be accompanied by an increase in HR
Why are old people more likely to get orthostatic hypotension (big drop in BP when they stand, making them momentarily lightheaded)?
Aging-> some baroreceptor activity is lost
*normally: you stand-> gravity is working against you so vessels have to constrict in the lower extremities to ‘milk’ blood up to the heart so it can pump enough to maintain BP. For the moment that BP is dropped right when you stand, baroreceptors (on carotid sinus) respond to decreased stretch-> decrease firing-> this increases sympathetic stimulation to raise the BP to baseline.
Young man faints when exercising. Has a crescendo-decrescendo systolic murmur in the left sternal border. Diagnosis?
HOCM
Basically a functional aortic stenosis, since the intraventricular septum is in the way of aortic outflow
IV drug user had an episode of syncope. Has a diastolic murmur at the left sternal border. Platelet count is elevated and EKG shows 2nd degree AV block. Diagnosis?
Perivalvular abscess
*Be suspicious of perivalvular abscess anytime a patient has endocarditis + conduction abnormalities on EKG (the abscess can extend into the conduction pathway, messing it up). Endocarditis alone wouldn’t cause AV block or syncope.
Man comes in for palpitations and SOB on exertion. He recently binge drank. HR is 130. EKG shows no clear P waves. Echo shows EF=35%, mitral regurg, and dilated LA and LV with global hypokinesis. What’s going on?
Alcohol-> A-fib w/ RVR (rapid ventricular response)-> tachycardia-mediated cardiomyopathy (the prolonged arrhythmia and rapid ventricular rate is causing HF)
*treat with aggressive rate and rhythm control
**note: the mitral regurg in this patient is just due to the fact that the ventricles are overloaded
What is tachycardia-mediated cardiomyopathy? How do you treat it?
When you have a tachyarrhythmia (heart is beating super fast, out of rhythm for a while) that leads to HF
(*can be due to a-fib, a-flutter, v-tach, etc.)
Treat with aggressive rate or rhythm control
(*AV nodal blocking agents, antiarrhtymic drugs, ablation of arrhythmia, etc.)
Lady presents with stroke symptoms. Over the past several months, she has had palpitations, SOB on exertion, and hemoptysis. Most likely explanation?
Rheumatic heart disease-> mitral stenosis-> a-fib-> stroke
*remember that mitral stenosis (MS) over time-> increased LA pressure. This predisposes to a-fib. This also leads to pulmonary vascular congestion, explaining the hemoptysis.
What is “flash pulmonary edema?”
Acute pulmonary edema secondary to increased cardiac filling pressures (such as after an MI)
Patient has episodes of squeezing chest pain at rest. EKG and exercise stress test are normal. Most likely diagnosis?
GERD
Gold standard for diagnosing type 2 DM in PCOS patients?
Oral glucose tolerance test
It is more sensitive in PCOS patients than fasting glucose and A1c standard screenings tests
Pathophys of PCOS?
Inc LH (related to insulin resistance)—> theca cells in ovaries use this to make androgens, then granulosa cells of ovaries take the androgens and make estrogen (estradiol).
With all the excess LH, there’s too many androgens for the granulosa cells to convert to estradiol, so excess androgens circulate in the blood and go into the peripheral fat—> fat cells make it into estrone and this feeds back onto the GnRH axis, inhibiting it.
Excess androgens—> hirsutism
Inhibition of GnRH—> anovulatory, infertile
55 year old guy has urinary frequency, urgency, hesitancy, and low back pain + perineal pain during ejaculation. The prostate is smooth but slightly enlarged. Urine culture is negative. Most likely diagnosis?
Chronic prostatitis
(Noninfectious chronic prostate inflammation)
- this is a diagnosis of exclusion based on urinary symptoms + perineal or genital pain + pain or blood with ejaculation in the setting of a negative urine culture
- antibiotics (fluoroquinolones) can help (even though a bacteria is not identified)
- alpha-adrenergic inhibitors (Tamsulosin) and 5-alpha-reductase inhibitors (Finasteride) can also help
How does epididymitis (inflammation of the epididymis of the testicles) typically present?
Urinary/ voiding symptoms + scrotum pain/ swelling + purulent (pus) urethral discharge
Why would you test a patient with Raynaud phenomenon for autoantibodies and inflammatory markers (ex: ANA)?
It can occur in the setting of an autoimmune or systemic disease (ex: CREST syndrome)
What drugs may be helpful for Raynaud phenomenon?
Dihydropyridine CCBs
Vasodilate, so help improve perfusion to the fingertips
Lichen planus (pruritic, purple, papules, plaques) is associated with what disease?
Hepatitis C
If FENa (fraction of excreted sodium) is >2%, what does that tell you?
It’s either post-renal (later stage) or intrinsic AKI
Normal FeNa= <1%. If FeNa is higher, you know the kidneys are not working to reabsorb Na+
Lady has pyelonephritis. Later develops intrinsic AKI. What agent was she likely treated with?
An aminoglycoside
-these drugs treat serious gram-negative infections (pyelonephritis is often due to E-coli—a bladder infection that ascends) and are nephrotoxic
Minimal bright red blood per rectum (not mixed in stool) is most often due to benign disorders such as __________ and __________.
Hemorrhoids (varicose veins in the rectum that can cause bleeding) OR Anal fissures (aka anal ulcer) (small tear in the lining of the anal wall)
What is a barium enema?
They give you a contrast solution and then take an x-ray of the colon
Patient under 40 years old has minimal bright red blood per rectum. What test should you do first?
Anoscopy (anal speculum)
Why? This is minimally invasive and allows you to look in there for hemorrhoids (varicose veins) or rectal fissures (ulcer/ tear in anal wall). If you don’t find the cause with the anoscopy, then consider a sigmoidoscopy or colonoscopy.
*If the patient were 40-49, you may consider a sigmoidoscopy. If the patient were 50+ and it’s been 2-3 years since the last colonoscopy, you’d want to do a colonoscopy.
How long does a seizure have to go on for there to be risk of permanent brain injury?
> 5 minutes
*Status epilepticus used to be defined as a seizure <30 min, but recent studies show all it takes is 5+ minutes of seizing for there to be risk of permanent brain injury (from the excitatory cytotoxicity)
How do we get rid of Basal Cell Carcinoma (pearly nodules) on the face and other cosmetically sensitive areas?
Mohs micrographic surgery
(Sequential removal of thin layers of skin with microscopic inspection to confirm that the margins have been cleared of malignant tissue)
Name for brown plaques/ nodules with “stuck-on” appearance?
Seborrheic keratosis
Drug-induced acne is a common side effect of what drugs?
Corticosteroids
If a patient cannot run on a treadmill, how do we do a stress test?
Give them Adenosine (vasodilator)
- to normal coronary arteries—> this causes a big increase in blood flow (dilates them a lot)
- to stenotic coronary arteries—> this does not cause an increase in blood flow (the body’s mechanisms have already dilated these stenotic vessels to the max, so adding in a vasodilator doesn’t do a thing)
- the difference in blood flow allows us to diagnose CAD
Guy has an MI. You also notice an S3 heart sound and crackles in the lungs on examination. He’s already been given ASA, Clopidogrel, and Atorvostatin. What should you give him next?
Furosemide
-Diuretics are recommended for acute pulmonary edema (“flash pulmonary edema”) secondary to an MI.
*Although beta-blockers are part of the therapy for MI (“MONA BASH”), do NOT give a beta-blocker to a patient with decompensated CHF (dilated cardiomyopathy) or bradycardia
(This guy has this based on S3 and crackles—fluid overloaded). Why? Beta-blockers cause decreased contractility and HR…if you already got a pumping problem, this will worsen it!
What lung conditions are associated with CREST syndrome?
Interstitial fibrosis and pulmonary HTN
*if pulm HTN, would expect a RV heave (impulse palpated immediately left of the sternum that suggests RV enlargement) and/or a loud pulmonary component of the 2nd heart sound
Girl with hx of depression and chronic back pain overdosed on meds in a suicide attempt. Has a seizure on her way to the ED. She’s tachy, hypotensive, skin is warm and flushed, pupils dilated, bowel sounds decreased, and QRS prolonged.
What did she overdose on and what are you going to do about it?
TCA (tricyclic antidepressants) overdose
Give sodium bicarbonate
*Can cause QRS prolongation (or QT prolongation-> Torsades). Also causes anti-cholinergic effects.
Calcium gluconate is given in what arrhythmia?
Hyperkalemia (peaked T waves)
Homeless guy comes in smelling like alcohol. BP is 90/60, HR 95, RR 5. Has normal pupil size. Extremities are cool to touch. Decreased bowel sounds and muscular tone. Diagnosis? What is your priority in managing this patient?
Opioid overdose
Priority= airway protection—intubate and give Naloxone (mu-opioid antagonist to reverse acute opioid toxicity)
- What gives it away is the respiratory depression (RR=5)!
- Other findings also support this diagnosis (extremities cool to touch is due to hypothermia from impaired thermogenesis)
*don’t rule out opioid use just cuz the pupils are normal sized (not pinpoint)! They can be normal (could even be dilated if the patient took amphetamines too, for example)
What do you give for beta-blocker overdose/ intoxication?
Glucagon!
What’s a “scaphoid stomach?”
A sunken in stomach
Teenage girl has constipation and says her stomach is “puffed up.” She has cold intolerance. BP and HR are low. BMI is 18. On exam, abdomen is non-distended and normal bowel sounds. Diagnosis?
Anorexia nervosa
BMI <18.5 + distorted body image (thinks stomach is “puffed up” when it is not)
- Constipation and cold intolerance are also consistent with hypOthyroidism. BUT, in hypOthyroidism you’d expect weight GAIN (everything is slowed down) and HTN (not low BP).
- In Anorexia, electrolyte abnormalities—> slowed bowels and constipation. Malnutrition—> loss of muscle mass (which includes the heart)—> heart shrinks and beats slower to conserve energy (think of it as the heart is weakened bc it is starving)
Treatment options for psoriasis?
Topical glucocorticoids (betamethasone, fluocinonide) or Vitamin D derivatives
Another name for esophagogastroduodenoscopy (EGD)?
Endoscopy
Tube that goes down the mouth-> esophagus-> stomach-> duodenum
Guy with HTN (taking a Thiazide diuretic) is peeing all the time, thirsty all the time. Glucose is 90, Na+ is 150, serum osmolality is 300, urine osmolality is 125. Most likely diagnosis?
Diabetes insipidus (DI)
- glucose is normal, so rule out DM
- Na+ is high, so rule out side effect of the Thiazide diuretic alone (this causes hypOnatremia)
- the blood is more concentrated than the urine…in DI, you are not making/ responding to ADH, so you cannot retain water and just pee it all out, makes sense
Lady complains of daily headaches. She used to get migraines a lot and uses over-the-counter analgesics (pain relievers for headache, like Tylenol) each day. What advice should you give her?
Stop taking the over-the-counter headache meds!
Using these too often—> medication overuse headaches (like a caffeine headache, these occur do to getting addicted to the meds)
Why do you get chills with fever?
Fever-> cytokines cause the hypothalamus to change the body’s setpoint to a higher level-> to reach this new setpoint, peripheral blood vessels vasoconstrict (to shunt blood to the core) and this can make a person feel cold
*also, muscles may contract (shivering) during this process
Patient comes in for recurrent sinusitis. He also has hematuria, found on urinalysis. Past medical history is significant for chronic joint and back pain. Likely diagnosis and next best step?
Granulomatosis with polyantiitis (Wagner’s)
- small-vessel vasculitis involving the nasopharynx, lungs (but not in this patient), and kidneys
- systemic symptoms are common (anemia, fatigue, fever, joint pains)
Next step= check for c-ANCA (autoantibodies against neutrophils)
*tissue biopsy is the confirmatory test
What test can you do to confirm lactose intolerance and how does it work?
Hydrogen breath test
- Lactose intolerance= you lack lactase, a brush border enzyme that breaks down lactose in dairy products (decreases with age, esp in Asians). Since lactose doesn’t get broken down into simple carbs, its draws in water-> osmotic diarrhea.
- Since it’s not broken down, more stomach acid will try to compensate to digest it—> positive H+ breath test.
High, low, or normal osmotic gap in lactose intolerance?
High
Old lady just diagnosed with colon cancer comes in complaining of intermittent pressure-like chest pain since the morning. EKG shows T wave inversion in leas V2-V4. Angiogram shows no blockage. Diagnosis?
Stress-induced (takotsubo) cardiomyopathy
Aka “broken heart syndrome”
- believed to be brought on by a catecholamine surge from a stressor-> microvascular spasm and impaired contraction of the heart (hypokinesis).
- EKG usually shows evidence of ischemia (ST elevation, T wave inversion, etc.) in the anterior precordial leads (V1-V4) and troponin may be a little high. But, angiogram shows no CAD.
- self-limiting in weeks
EKG changes in:
- Panic attack
- Stress-induced cardiomyopathy (“broken heart syndrome”)?
- Panic attack—> no EKG abnormalities
2. Broken heart syndrome—> ischemic EKG symptoms (ST elevation, T wave inversion, moderately elevated troponin, etc.)
Are the following levels high, low, or normal in Paget’s dz of the bone?
- Serum calcium
- Serum phosphorus
- Alkaline phosphatase
- Urgent hydroxyproline
- Serum calcium- NORMAL
- Serum phosphorus- NORMAL
- Alkaline phosphatase- HIGH
- Urgent hydroxyproline- HIGH (an elevated bone turnover marker)
- Paget disease of the bone- imbalance between osteoclast and osteoblast function (osteoC’s go crazy breaking down bone w/o the regulation of osteoB’s-> osteoB’s rush to compensate and lay down bone, but do a poor job of it-> thick bone that fractures easily)
- Symptoms: bone pain, increasing hat size, hearing loss, lion face, isolated elevated alk phos (due to activation of osteoB’s)
Lady in the ED has an S3 and bilateral crackles. O2 sat is 78% with 40% oxygen, so she is intubated for respiratory failure and given nitrates and diuretics. Breath sounds on the left continue to be decreased. How can you restore them?
Reposition the endotracheal tube
(When you intubate, the goal is to get the tube just before the carina, where the main bronchus bifurcates into the right and left bronchus. If only one lung is expanding after intubation, you advanced the tube too far into either the right bronchus or the left bronchus.)
Patient had a URI 2 weeks ago that resolved. Now he has tingling in his foot, bilateral muscle weakness, and absent knee and ankle reflexes. No headache or photophobia. Diagnosis?
Guillain-Barré syndrome
-ascending paralysis from a URI or diarrheal illness (Campylobacter jejuni)
Will the following be high, low, or normal on examination of CSF in a patient with Guillain-Barré syndrome? Protein WBC’s RBC’s Glucose
Protein- HIGH
WBC’s- NORMAL
RBC’s- NORMAL
Glucose- NORMAL
- CSF protein may be high due to increased permeability of the blood-nerve-barrier
- treat with IV Ig or plasmapheresis
- takes patients months to recover (can be chronic too- I saw a patient like this in the hospital)
When is it ok to accept a gift from a medical conference?
When the gift directly benefits patient care and it is of low monetary value
What are the indications for long-term home oxygen therapy? What about in patients with cor pulmonale, right HF, or hematocrit >55%?
- PaO2 < 55 or oxygen sat SaO2 < 88%
- In patients with cor pulmonale, right HF, or hematocrit >55%, PaO2 < 59 or oxygen sat SaO2 < 89%
- *PaO2= Oxygen in blood, not bound to Hb
- *SaO2= Percent of oxygen that is bound to Hb (saturated)
What do you do with a patient who has an epidural hematoma?
Emergent neurosurgery to get rid of the hematoma
A patient is having an MI. What’s the max time you can take to place that stent (PCI)?
90 min
Middle age man has nerve palsy, low-grade fevers, enlarged parotid glands, enlarged cervical lymph nodes. Labs are normal, except calcium is high. He is sexually active with multiple women. Diagnosis?
Sarcoidosis
-systemic granulomatous disease that can involve the nervous system (Bell’s palsy), lymphadenopathy, parotid gland swelling, hypercalcemia (1-alpha hydroxylase activity)
What EKG chance does TCA (tricyclic antidepressant) overdose cause?
TCAs block fast sodium channels—> slower conduction speed= QRS prolongation
(*can also lead to Torsades)
*Treat with sodium bicarb bc it increases serum pH (more alkaline) and extracellular sodium. Both the increased pH and extra extracellular Na+ decrease the drug’s binding to cardiac Na+ channels.
Normal calcium level?
8.4-10.2
For simplicity, remember about 8.5-10
Patient has breast cancer that metastasized to bone. She had a mastectomy and is undergoing chemo.
She is having vague bone pain. Has a palpable supraclavicular lymph node and high calcium.
What is this and how do you treat it?
Hypercalcemia of malignancy
Bisphosphonates
She has metastatic breast cancer to the bone—> more bone breakdown—> bone pain and higher levels of calcium in the blood (you can also get hypercalcemia of malignancy if you have a tumor secreting PTHrP).
Bisphosphonates cause osteoClast apoptosis so they can’t keep breaking down bone
Patient has an adrenal mass, high BP, headache, and hypokalemia. Diagnosis?
Primary hyperaldosteronism due to adrenal adenoma
*aldosterone-> Na+ reabsorption, K+ and H+ wasting, so hypokalemia makes sense
**treat with an aldosterone antagonist (Spironolactone, Eplerenone) or surgery
Old man has weakness and pain in his shoulders since shoveling snow 3 weeks ago. There is weakness on shoulder aBduction and decreased sensation on left forearm. Next step?
Get an MRI of the cervical spine
-He most likely has C5-6 nerve root impingement (cervical radiculopathy) from underlying cervical spondylitis (wear and tear of spinal disks in neck/ cervical spine degeneration)
Man has 1 year history of diarrhea, cramps, flushing, systolic murmur over left sternal border that increases with inspiration, and high LFTs. Diagnosis?
Carcinoid syndrome
- Serotonin-secreting tumor
- Usually in the GI tract, but if Mets to the liver, it can’t be broken down and serotonin travels through the bloodstream causing systemic effects. Can affect right heart only (tricuspid regurg in this patient) bc lungs (like the liver) have the enzyme to break down serotonin.
- Symptoms= diarrhea, flushing, tricuspid regurg, bronchospasm
How can Carcinoid tumors lead to Niacin (vit B3) deficiency?
Carcinoid= serotonin-secreting tumor Tryptophan gets used up to make serotonin Since tryptophan (and vit B6) are required to make niacin (vit B3), you’ll get a niacin deficiency as a result
Lady with hx of DM presents with sudden-onset double vision and ptosis of her right eye. The right eye is down and out. Pupils are responsive and there are no other neuro defects. Most likely diagnosis?
Diabetic ophthalmoplegia- poorly controlled DM—> ischemic neuropathy (tiny blood vessels that supply CN 3 are damaged)—> CN 3 palsy
Tendon vs. ligament?
Tendon- muscle to bone
Ligament (“Like”)- bone to bone
What is enthesitis?
Inflammation and pain at sites where tendons (muscle to bone) and ligaments (bone to bone) attach to bone
- most often at the Achilles’ tendon (but also can be at the costosternal junction, shoulders, elbows, hips, iliac crests, tibial tuberosities, etc.)
- can be part of an isolated disorder (like plantar fasciitis) or in spondyloarthropathies (like ankylosing spondylitis)
30 year old guy has low back pain that improves with use. He has limited spine flexion and sacroiliac joint inflammation. Has also had diarrhea going on. Diagnosis?
IBD (Crohn’s or Ulcerative Colitis)
*remember they are associated with arthritis, including spondylarthritis or sacroilitis
What does a positive pronator drift test tell you?
There is upper motor neuron (UMN) or pyramidal/ CST (corticospinal tract) disease
*UMN lesions cause more weakness in supinator muscles compared to pronator muscles of the upper limb—> affected arm drifts down and the palm turns (pronates) toward the floor
Middle aged woman is having strong urges to urinate and sometimes leaks urine on her way to the bathroom. What med can you give her?
Oxybutynin (anti-muscarinic for treatment of urinary incontinence)
What is presbycusis?
Age-related hearing loss
*due to cochlear hair cell loss (and cochlear neuron degeneration)
What can you advise patients to do when they get vasovagal syncope episodes- when they feel fainting coming on (prodromal phase)?
Cross legs, tense calf muscles, handgrip, and tense arm muscles with clenched fists…)
-These maneuvers increase venous return to the heart (more ‘milking’ of blood to heart)—> more CO, which can stop the syncope from happening
Fever and chills 1-6 hrs after blood transfusion. What reaction is this?
Febrile nonhemolytic transfusion reaction
(Due to cytokines in stored blood products)
*prevention of this is by leukoreduction of blood products (filter out most the WBCs after blood collection, before storage to prevent cytokine production within the packed RBC product)
What 2 medication classes can lead to severe hypotension if combined with a PDE-5 inhibitor like Sildenafil (Viagra) for ED?
- Nitrates
2. Alpha blockers (ex: Doxazosin)
Patient has fever and new holosystolic murmur at the apex. He was treated empirically with vancomycin. Blood culture results came back sensitive to penicillin. What should you change his antibiotics to (2 options)?
IV Penicillin G or IV Ceftriaxone
- Fever + murmur suggests endocarditis
- Initial emperic treatment with Vanco is appropriate to cover MRSA (just in case)
- Now we got cultures back and know it is not MRSA (it is sensitive to penicillin), so switch to IV penicillin or Ceftriaxone (easier to administer due to once daily dosing vs. every 4-6 hrs)
- Do not use oral Penicillin- should treat IV for endocarditis
Do you have a high A-a gradient in PE (pulmonary embolism)?
YES
You have a high A-a in any V/Q mismatch where there is impaired gas exchange!
- in the case of PE, the problem is with Q (perfusion)
- oxygen is getting from the alveoli fine, but the blood isn’t there to pick it up bc it is stuck (there’s a clot in major pulmonary vessels)
Do patients with PE typically have a high or low PaCO2?
LOW
PE—> hyperventilation (in effort to compensate)—> blowing off more CO2, so less CO2 stays behind in the blood
1st line treatment for female pattern hair loss?
Topical Minoxidil
A vasodilator that increases blood flow to the scalp
*side effects: irritation and itching
Old lady with PMH of DM and HTN has began having difficulty planning meetings for 9 months. She can no longer cook for herself. Gait is unsteady. She is sad. Diagnosis?
Vascular dementia
(Stepwise/ gradual decline, often presents with motor, gait, urinary, and psych symptoms)
*not likely to be Alzheimer’s bc that starts with memory problems and other stuff goes later
Patient flexes right hip and knee and slaps foot to ground w/ each step. He is complaining of recurrent falls. Cause of gait abnormality?
Common peroneal neuropathy
(L5 radiculopathy-> back pain radiating to the foot and weakness on foot inversion and plantar flexion)
*remember the common peroneal (fibular) nerve:
PED= Peroneal Everts and Dorsiflexes
If injured-> foot dropPED
Patients with SOB due to CHF have high BNP levels, typically above what number?
BNP >400
(Remember BNP is released by the heart in response to stretch, which there is more of when you have CHF and are fluid overloaded)
*BNP is a highly sensitive test for CHF. Clinical signs (JVD, crackles, lower extremity edema) are highly specific, but not sensitive.
Why might a male with a prolactinoma have decreased testosterone levels?
HIGH prolactin will feedback on GnRH, making it LOW (negative feedback)—> LOW testosterone production
35 year old guy has recurrent headaches. BP is 190/100 and you hear a S4 and continuous murmur. Diagnosis?
Coarctation of the aorta
- narrowing of descending aorta-> pressure overload in proximal part of aorta-> HTN in arms (where BP is normally measured), headaches (pressure goes back to carotids-> head)
- murmur for coarctation is systolic (blood through constricted aorta like aortic stenosis) or continuous (if collateral vessels are present)
- S4 may be heard due to LV hypertrophy (induced by HTN)
What may be seen on CXR of a patient with coarctation of the aorta?
Notching of the ribs (erosions of inferior costal surfaces)
-this finding is due to collateral vessel formation
Patient has watery diarrhea, flushing, and low K+ causing muscle cramps. CT shows a mass in the pancreatic tail. Diagnosis?
VIPoma
-rare tumor of pancreatic cells—> releases vasoactive intestinal peptide (VIP)
Patient has fever, acute-onset respiratory distress, hypoxemia, and bilateral opacities on CXR. Diagnosis?
ARDS (Acute Respiratory Distress Syndrome)
*acute inflammatory response w/ cytokines in the lungs-> epithelial damage/ necrosis of alveolar cells + endothelial damage/ inc capillary permeability leaking proteins-> hyaline membranes
What happens in ARDS?
Acute inflammatory response w/ cytokines in the lungs-> epithelial damage/ necrosis of alveolar cells + endothelial damage/ inc capillary permeability leaking proteins-> hyaline membranes
(The release of cytokines/ overreactive inflammatory response to a stressor like sepsis, PNA, whatever is the problem…causes damage to lung tissue)
**rarely can lead to irreversible pulmonary fibrosis (from too much collagen deposition as endothelial cells, pneumocytes, and fibroblasts proliferate to repair damaged lung)
What are the 2 ways to improve oxygenation in a ventilated patient?
- Increase FiO2 (fraction of inspired oxygen)
- Increase PEEP (positive end-expiratory pressure)
* This is the best way to improve hypoxemia in a patient with ARDS bc it additionally prevents alveolar collapse
If high levels (>60%) of FiO2 are required to maintain oxygenation in a patient on a ventilator, what setting should you increase?
PEEP (positive end-expiratory pressure)
- There are 2 ways to improve oxygenation of a ventilated patient:
1. Increase FiO2 (fraction of inspired oxygen)
2. Increase PEEP (positive end-expiratory pressure)
Patient has nasal breathing, stuffy nose, dry cough for more than a year. No allergies. Diagnosis and treatment (2 options)?
Nonallergic rhinitis (aka vasomotor rhinitis)
Treat with an intranasal antihistamine and/or intranasal glucocorticoid
Man comes in after long plane flight with LUQ pain. Has high indirect bilirubin (UCB), high reticulocyte count, and splenomegaly. Most likely cause of his symptoms?
Splenic infarction
(Acute occlusion of splenic artery, causing LUQ pain)
- High retic count and UCB= Intravascular hemolysis
- Could be due to sickle cell trait (usually asymptomatic, but can get Intravascular hemolysis and splenic infarction in stressors like a long flight- do Hb electrophoresis to diagnose
What is “salvage therapy?”
Treating a disease a different way when the standard treatment fails
(Ex: guy gets radical prostatectomy for prostate adenocarcinoma and PSA is undetectable. Months later, PSA is high and he gets radiation= a salvage therapy)
Old guy has progressive loss of vision in his right eye. Vertical lines look bent and wavy to him. Diagnosis?
Macular degeneration
- often age-related, the macula (center of retina in back of eye responsible for visual acuity) wears down
- early finding= straight lines look wavy
- eventually they loose central vision
*most common cause of blindness in industrialized nations
How do we confirm a diagnosis of Scabies and how do we treat it (2 drug options)?
Diagnosis: light microscopy of skin scrapings
Treatment: topical permethrin or oral ivermectin
30 y.o. African American woman
Painful, stiff hands/ wrists, esp in morning
Muscle aches
Ulcer on buccal mucosa
Lymphadenopathy
Low Hb (anemia), low platelets (thrombocytopenia)
Diagnosis?
Lupus (SLE)
Diagnosis if 4+ of these criteria:
- Butterfly rash
- Photosensitivity
- Oral/ nasopharyngeal ulcers
- Discoid rash (coin-shaped, worse with sun exposure)
- Arthritis
- Pericarditis
- Hematologic dz (anemia, leukopenia, thrombocytopenia)
- Renal disease (proteinuria, casts)
- CNS- seizures, psychosis
- Immuno markers (false positive Syphilis, anti-dsDNA, anti-Smith Ab)
- ANA
*She has: (1) arthritis, (2) oral ulcer, (3) lymphadenopathy, (4) anemia and thrombocytopenia
What is Felty syndrome?
Triad of:
RA + splenomegaly + neutropenia (low neutrophils-> high-risk for bacterial infections)
*“SANTA’s suit is felty” Splenomegaly, Anemia, Neutropenia, Thrombocytopenia, Arthritis (Rheumatoid)
Patient who got a liver transplant 5 months ago (taking immunosuppressants, no antibiotics) comes in with SOB, nonproductive cough, fever, chills. O2 sat is 82%, has bilateral crackles, diffuse interstitial infiltrates, elevated lactate dehydrogenase (LDH).
What test should you order?
Bronchoalveolar lavage
This is likely PCP (Pneumocystis) pneumonia
*immunosuppressed/ organ transplant patients are at high risk for PCP and CMV pneumonia. Therefore, they should be on prophylactic Bactrim (for PCP) and Ganciclovir-Valganciclovir (for CMV in seropositive patients)
What does recumbent mean?
Lying down
Guy smoker has blood in urine and fever for 4 weeks. Family hx of blood disorder. Has a left-sided varicocele even when lying down.
Next test?
Abdominal CT
- Patient most likely has RCC (renal cell carcinoma) (*classic triad: flank pain, hematuria, palpable abdominal mass is in few patients)
- smoking is a risk factor
- varicocele is due to tumor pressing against left renal vein and left testicular vein, impairing venous drainage from testicle
- fever is a nonspecific cancer finding (also weight loss, anorexia, fatigue, night sweats)
- ectopic production of EPO by kidney tumor-> polycythemia
Increased QRS voltage (really high QRS peaks) tells you what?
LV hypertrophy
Guy has narrowed retinal vessels and blurred vision and increased QRS voltage on EKG and T wave inversion. BP is 130/80.
What’s going on?
Isolate ambulatory HTN (aka masked HTN)
- even though BP is okay rn, it is probably high on average (avg over day of >135/85= HTN)
- he has evidence of end-organ failure from HTN (retinal AV nicking aka hypertensive retinopathy and LV hypertrophy shown by peaked QRS’s)
Woman had 2 miscarriages. Positive VDRL. Low platelets (thrombocytopenia). High PTT.
Diagnosis?
Treatment?
Anti-phospholipid antibody syndrome
Treat/ prophylaxis with aspirin and LMWH (low molecular weight heparin) to avoid clotting problems and pregnancy loss
- the presence of antiphospholipid antibodies + you have blood clots (DVT, PE, stroke, MI) or pregnancy problems (miscarriages or premature birth from placental insufficiency or preeclampsia)
- antiphospholipid antibodies are seen in SLE (but not specific to it). They can cause 3 problems: (1) antiphospholipid antibody syndrome, (2) increased PTT, (3) false positive syphilis test (RPR, VDRL)
Guy has cough, fatigue, unintentional weight loss, enlarged mediastinum, enlarged hilar and mediastinal lymph nodes.
PET (positron emission tomography) scan with 18-fluorodeoxyglucose shows uptake in the brain, kidneys, bladder, supraclavicular and mediastinal lymph nodes.
Diagnosis?
Hodgkin lymphoma
- B symptoms
- painless lymphadenopathy
- mediastinal mass
- PET scan radiotracer is taken up by cancer cells w/ a high metabolic rate (supraclavicular and mediastinal LN’s) and healthy organs with high metabolic rates (brain, kidneys, bladder)
Guy has diverticulitis and gets treated. A couple days later, he develops acute pain and redness in his right ankle (had a similar episode before). Diagnosis?
Gout
- usually occurs in big toe, but can occur in ankle or knee too
- triggers: alcohol, surgery/ trauma, dehydration, some meds (diuretics)
Explain what goes down when the RAA System is activated.
*triggers that activate RAAS: low BP, low NaCl delivery to macula densa, sympathetic NS kicks in
- Liver releases AT
- Kidney JGA cells release Renin, which converts AT-> AT I
- Lungs release ACE (angiotensin converting enzyme), which converts AT I-> AT II
* ACE also breaks down bradykinin - AT II has multiple effects on the body to raise BP:
- vasoconstriction
- constricts efferent arteriole (raise GFR)
- aldosterone release from adrenal gland-> reabsorption of Na+ (wasting of K+, H+)
- ADH (retains water) and thirst
Explain amaurosis fugax.
Temporary loss of vision (in 1 or both eyes)
-For example, due to emboli from severe carotid stenosis can cause ischemia to the optic nerve-> transient (on/off) vision loss
Young woman comes in with really high BP of 165/100 and transient (on/off) vision loss in an eye. She has a right carotid bruit. Renin and aldosterone levels are high. Next step?
CT Angiogram of the abdomen (look at the renal arteries)
Why? She has such a high BP that it is causing transient vision loss (amaurosis fugax- emboli from severe ipsilateral carotid stenosis can cause ischemia to the optic nerve), so you need to work it up. High Renin and Aldosterone means it’s secondary hyperaldosteronism. This is most likely due to FIBROMUSCULAR DYSPLASIA (developmental defect in blood vessel wall-> irregular thickening of renal, carotid, vertebral arteries)-> kidneys read low BP-> activate RAAS-> increased renin, aldosterone, and BP.
Atrioventricular (AV) nodal reentrant tachycardia (AVNRT) is a sub-type of what tachycardia?
Paroxysmal supraventricular tachycardia (PSVT)
What is the diving reflex? (Our body’s response to immersion in cold water)
Reflex on immersion in cold water that slows HR and causes peripheral vasoconstriction to divert blood flow to central, vital organs (brain, heart, lungs) to conserve oxygen until breathing resumes and to delay potential brain damage
(*the body knows it cannot breathe in oxygen while underwater, so it slows the HR down so that the body can survive longer with the blood/ oxygen it already has to pump)
colder water (drops core temp super fast)= stronger diving reflex response (and therefore better chance of survival if you drown in ice cold water vs. a pool)
(supraventicular means it is coming from the atria)
How would immersion in cold water relieve heart palpations? (state mechanism involving baroreceptors)
Vagal maneuver (cold water immersion/ diving reflex, carotid sinus massage, Valsalva, eyeball pressure)—> increased stretching and firing of baroreceptors—> more parasympathetic response—> lowered HR
*diving reflex (immersion in cold water slows the heart to conserve energy/ so you could survive longer + vasoconstricts to shunt blood to central, vital organs)
In hypovolemic shock, are the following values high or low?
- pulmonary capillary wedge pressure (PCWP)
- cardiac output (CO)
- blood pressure (BP)
- systemic vascular resistance (SVR)
- PCWP (=LA pressure)- LOW (due to decreased preload)
- CO- LOW (due to decreased preload)
- BP- LOW (due to deceased CO)
- SVR- HIGH (vasoconstriction in attempt to raise BP and maintain CO)
Why might an inferior MI (ST elevations in II, III, aVF) cause AV block (prolonged PR intervals w/ dropped QRS’s)?
Inferior MI—> occluded RCA, which supplies the AV node—> since the AV node has cut off blood supply, it won’t be able to do a good job of delaying the signal from the atria to ventricles—> AV block
(prolonged PR’s= impulse from atria to ventricles gets too delayed, dropped QRS’s= part of the AV node is blocked so failing to send the impulse from the atria to ventricles)
60 y.o. smoker has sudden-onset chest pain, diaphoresis, and N/V. BP is 85/55 and HR is 50 bpm. EKG shows ST-elevations in leads II, III, aVF. Diagnosis?
Inferior MI- occlusion of the RCA
*His vitals tells you he’s in cardiogenic shock (really low HR and BP). This makes sense bc MI-> heart not getting fed enough blood to pump well
In pericarditis, what do you see on EKG?
Diffuse ST-segment elevations
Guy had an MI 3 days ago. Now he’s coming in with sharp pain on his left chest that improves with leaning forward. Diagnosis?
Acute pericarditis (aka fibrinous pericarditis aka peri-infarction pericarditis)
*EKG would show diffuse ST-segment elevation
Woman with history of rheumatic heart dz has acute onset SOB. She has a mid-diastolic rumble at the apex, crackles over the lungs, and EKG shows irregularly, irregular rhythm and no P waves. What’s going on?
She has mitral stenosis (from rheumatic heart disease which causes mitral regurg, later mitral stenosis)—> increased pressure in LA causes the LA to dilate—> predisposes to a-fib—> worsening flow through the stenotic mitral valve—> more backing up of blood/ congestion to lungs, explaining the SOB
*up to 70% of patients with mitral stenosis will develop a-fib from the significant LA dilation
Most reliable finding to differentiate between an epileptic seizure and syncope?
Tongue biting
(*95% specificity for epileptic seizure, esp if on the lateral tongue- bc rarely syncope can cause frontal tongue biting)
What are these EKG findings suggestive of?
High-voltage QRS complexes, lateral ST segment depression, and lateral T wave inversion
LV hypertrophy
30 year old guy has a nosebleed requiring nasal packing. His BP is 180/120. EKG shows high-voltage QRS complexes, ST-segment depression, and T-wave inversion. Most likely diagnosis?
Coarctation of the aorta
- high-voltage QRS’s, ST-segment depression, and T-wave inversion= LV hypertrophy from long-standing HTN
- prob not essential HTN bc that rarely causes end-organ damage in young patients <40
- coarctation of the aorta (narrowing at distal aorta) usually causes asymptomatic HTN, but can cause headache, nosebleeds, lower extremity claudication
*check bilateral arm and leg BP measurements
Old lady has acute-onset epigastric pain associated with N/V. What test should you do 1st?
ECG
*You need to rule out acute coronary syndrome (STEMI, NSTEMI, unstable angina), which could have an atypical presentation like this! Once ruled out, then you can consider GI things like pancreatitis
**women, elderly, and diabetes patients are more likely to have atypical heart symptoms
How is vasospastic (Prinzmetal) angina similar to Raynaud phenomenon?
Vasospastic (Prinzmetal) angina- due to episodic vasospasm of pulmonary vessels
Raynaud phenomenon- due to episodic vasospasm in fingers and toes
What is the screening protocol for AAA?
One-time abdominal ultrasound screen for men 65+ who have ever smoked
How do you treat Wolff-Parkinson White syndrome patients with A-fib with RVR:
- if unstable?
- if stable?
Unstable—> immediate cardioversion
Stable—> IV procainamide or Ibutilide (rhythm control)
*do NOT use AV node blockers like adenosine, beta blockers, CCBs, digoxin—they would promote conduction across the accessory ‘secret’ pathway, causing a-fib—> v-fib
Meniere disease is a disorder of the inner ear (too much endolymph/ fluid) characterized by what triad?
- Episodes of vertigo (20 min- 24 hrs, associated with nausea/ vomiting)
- Sensorineural hearing loss (fluctuates)
- Tinnitus (ringing of ear)
Woman comes in for episodes of dizziness (room spinning) associated with ringing in the ears, improved with lying down and eyes closed. When you do Rinne test, air conduction > bone conduction on both ears. When you do Webber test, the sound is heard better on the left. Diagnosis?
Meniere Disease (disorder of inner ear where you have too much volume/ pressure of endolymph fluid)
Triad:
- Episodes of vertigo
- Sensorineural hearing loss
- Tinnitus
You need 2/3 criteria to diagnose acute pancreatitis. What are they?
- Acute-onset epigastric pain radiating to the back
- Increased amylase or lipase >3x the upper limit of normal (lipase more specific)
- Abdominal imaging suggestive of pancreatitis- CT of abdomen (pancreatic enlargement)
* NOTE: you do NOT need CT to make the diagnosis…epigastric pain radiating to back + lipase >3x upper limit of normal is sufficient!
**U/S is not used (gas prevents visualization) and X-ray is not used (poor test for pancreatitis)
Guy has an NSTEMI (substernal chest pain w/ diaphoresis, ST depressions, up-trending troponin) so he gets a stent placed. Besides ASA, a beta-blocker, statin, ACE inhibitor, what do you need to give him?
A P2y12 receptor blocker
(like Clopidogrel aka Plavix)
*normally, ADP binds this receptor on platelets to promote platelet aggregation (we block it to stop platelet aggregation)
Dual Anti-Platelet Therapy (DAPT) (ASA + P2y12 receptor blocker) is given to patients with stents for 12 mo to reduce the risk of stent thrombosis. Also, it reduces risk of recurrent MI in NSTEMI compared to ASA alone!
If a patient gets a stent, how long do they need to be on DAPT (Dual Anti-Platelet Therapy= Aspirin + P2y12 receptor blocker like Clopidogrel/ Plavix)?
At least 12 months
Significantly reduces risk of stent thrombosis and recurrent MI
Younger guy who has a sore throat for 4 days is coming in due to hematuria. U/A shows protein and RBCs in his urine. Diagnosis?
IgA nephropathy
- protein in urine= nephrotic syndrome
- most common nephrotic syndrome in adults= IgA nephropathy, esp after a URI (“sore throat”)
Lady has right ear pain, red vesicles in the ear canal, and right facial droop. Diagnosis?
Herpes zoster oticus
aka Ramsay Hunt syndrome
Varicella zoster (VZV) reactivates—> Herpes zoster. If the herpes occurs in the dermatome of the geniculate ganglion (collection of sensory nerves from the facial nerve in the facial canal of the head), you get this. It disrupts CN 7/ facial nerve motor fibers and spreads to CN 8/ vestibulocochlear nerve—> facial paralysis and ear pain there.
Old man presents with worsening SOB and nonproductive cough. Has had an ongoing fever, headache, sore throat, runny nose, anorexia, and body aches since Christmas shopping at a mall 5 days ago. He has crackles. Diagnosis?
Influenza virus
(Muscle aches + nonspecific flu symptoms after shopping in a germy mall)
*pneumonia is the most common complication of the flu
Most common complication of influenza?
Pneumonia!
- This can be from secondary bacterial infection (ex: Strep pneumo, Staph a.) or from direct viral attack (influenza pneumonia)
- give oxygen support and oseltamivir (Tamiflu) + treat the pneumonia with Abx
50 y.o. Guy has nausea, fatigue, bilateral flank pain over the last couple yrs. BP is 160/100. Liver is large, mass is felt on palpation of flank, prostate is enlarged. BUN and Cr are high. Diagnosis?
Autosomal Dominant Polycystic Kidney Disease (ADPKD)—> chronic kidney dz (CKD)
- evidence of ADPKD: flank pain, HTN (would be due to excess renin release), large liver (cysts)
- evidence of CKD: nausea, fatigue, high Cr (due to structural degeneration of the kidneys)
- NOTE: BPH is a separate issue here
Car crash victim is having severe pain from a leg fracture. He is a former heroin addict. You give him ketorolac (NSAID) for pain management, but it doesn’t cut it. What do you give now?
IV Morphine
*INITIAL management for acute pain (including opioids) is about the same for all patients—regardless of addiction history (you will just need to monitor this guy closely to avoid relapse)
Why do you get the following in aortic stenosis?
- Diminished and delayed carotid pulse (“pulsus parvus et tarsus”)
- Systolic murmur (late-peaking, crescendo-decrescendo)
- Soft and single S2
- Diminished and delayed carotid pulse (“pulsus parvus et tarsus”)—> since you have a stenotic aortic valve, there’s less blood flow making it through
- Systolic murmur (crescendo-decrescendo)—> aortic valve opens during systole so makes sense that aortic stenosis (problem opening) is heard during systole
- Soft and single S2—> normally, you have physiologic split of S2 (inspiration-> more blood to right heart-> pulmonic valve takes slightly longer to close than aortic valve in S2)…with aortic stenosis, the stenotic aortic valve takes longer to close too so they close at the same time= single S2
40 y.o. guy comes in for a physical. He has fatigue, muscle aches, weight gain. His total cholesterol and triglycerides are high. What is the next best step to manage his dyslipidemia?
Order TSH
Fatigue, muscles aches, weight gain-> suspicious for hypothyroidism, which can cause lipid abnormalities!
You need to confirm this diagnosis—if it is in fact hypothyroidism, you will need to treat the underlying cause with Levothyroxine (will improve lipid levels, but does take a few months). Don’t jump straight to a statin (can worsen myopathy) or another anti-lipid drug until you do the work-up.
Mechanism responsible for angina pain relief with nitrates?
Decreased LV wall stress (afterload)
Nitrates-> venodilate-> decrease preload/ blood in heart-> decrease demand on the heart (heart has to pump less blood) to match decreased supply (heart fed less blood) from angina
*they also vasodilate, resulting in less pressure (afterload) the heart has to pump against
**nitrates-> decreased LV end diastolic volume and wall stress-> decreased myocardial oxygen demand
What is a proctocolectomy?
Surgical removal of the rectum and colon
Done in FAP and UC, for example
Kid has FAP (familial adenomatous polyposis). How do you manage it?
Frequent colonoscopic surveillance
- screening sigmoidoscopies for kids starting at 10-12 yrs
- once you detect adenoma (or if >50 yrs) do annual colonoscopies
- do proctocolectomy (surgical removal of rectum + colon) if they initially present bad with high-grade dysplasia or adenomas or once they get into their 20’s (prophylactic since nearly 100% FAP patients will get colon cancer)
Lady has sudden onset left-sided weakness. Has positive Babinski. Has fatigue and a mitral regurg murmur (holosystolic at apex). ANA (antinuclear antibody) and RPR (rapid plasma regain) are positive. Diagnosis?
Antiphospholipid antibody syndrome
(These antibodies are present in SLE/ lupus and we call it a syndrome if you also have blood clots or miscarriages/ placental problems)
-sudden-onset left-sided weakness= stroke
(Babinski= UMN signs)
-fatigue and mitral regurg are lupus symptoms (antibodies can damage valves-> exposure of subendothelial collagen-> vegetations of platelets/ clotting factors form)
-ANA is non-specific to autoimmune dz’s
-false positive Syphilis (RPR/ VDRL) is a thing with antiphospholipid antibody syndrome (*as well as high PTT)
What 2 types of pneumonia should you be suspicious of in an immunocomprimised pneumonia patient?
- CMV (cytomegalovirus)
2. PCP (pneumocystis)
Tachycardia…
Narrow QRS, what is it?
Wide QRS, what is it?
Narrow QRS—> SVT (supraventricular tachycardia) or A-fib
*In SVT, the fast rhythm is coming from the atria. QRS is narrow (shorter ventricular contraction) bc it the atria send a rapid signal to the ventricles-> ventricles contract faster, keeping up with incoming signals.
Wide QRS—> V-tach (ventricular tachycardia) or Torsades
*In V-tach, the fast rhythm is coming from a rapid-firing pacemaker in the ventricles. QRS is wide (takes longer for ventricular contraction) bc it takes longer for a signal to go from ventricular myocyte to myocyte over the normal conduction pathway. That said, since it’s not paying attention to atrial signals and the ventricle is just going crazy on its own, the overall pace is fast/ tachy.
How do you treat SVT (supraventricular tachycardia) (narrow QRS) if the patient is stable? Unstable?
Stable SVT—> Adenosine (x3, rate control)
Unstable SVT—> shock
- Sketchy: Adenosine (swing dancing) is the agent of choice of SVT
- *Valsalva, carotid sinus massage, breath holding, and immersion in cold water may help temporarily by lowering HR
How do you treat V-tach (wide QRS) if the patient is stable? Unstable?
Stable V-tach—> Amiodarone
Unstable V-tach—> shock
Panic attacks usually cause what type of tachycardia?
Sinus tachycardia
Normal P waves followed by QRS’s
*do NOT cause narrow QRS= supraventricular tachy (PSVT) or wide QRS= V-tach
In paroxysmal supraventricular tachycardia (PSVT) will you see P-waves?
No, probably not
You get narrow QRS complexes and can have “hidden P-waves”
Lady had an MI of the LAD. Got a stent. On day 4 of hospitalization, she develops SOB, confusion, cold extremities, JVD, crackles. Has a loud systolic murmur at the left sternal border with a palpable thrill. What happened?
Rupture of the interventricular septum
- can happen 3-5 post-MI of the LAD or RCA
- when the interventrciular septum ruptures you basically get a VSD with flow from the LV-> RV, which explains the holosystolic murmur and cardiogenic shock presentation (too much backward flow of blood, not enough forward flow)
Where is aortic regurg heard best?
The left sternal border
(Not the usual right 2nd intercostal space where you hear many aortic murmurs echo best…aortic regurg is actually heard best directly over the aortic valve)
What should you think of when you hear flashes, floaters, or curtain across vision?
Retinal detachment
Does the retina share a blood supply with the macula?
No! They have their own blood supply
Patient has both a metabolic acidosis from AKI (kidneys not working to reabsorb bicarb-> low bicarb in blood) and respiratory acidosis from hypoventilation (breathe less-> blow off less CO2-> high CO2 in blood). The patient feels lethargic. What is the lethargy due to?
The respiratory acidosis/ CO2 retention (hypercapnia)
Why can AKI cause metabolic acidosis?
The kidneys aren’t working to reabsorb bicarb-> less bicarb in the blood
What is the CURB-65 scoring?
MD Calc tool to determine whether a pneumonia patient should be admitted to the hospital
C- confusion (+1) U- urea >20 (+1) R- respirations >30/ min (+1) B- BP, hypotensive <90/60 (+1) Age >65 (+1)
If CURB-65 score is 3 or greater—> admit to hospital (*if 1-2 you might still admit)
**basically you’re looking at their vitals (is this a sepsis-like picture, really sick patient?) to determine if they need inpatient vs outpatient care
What should you give a patient with CAP admitted to the hospital floor (bc they are really sick)?
Beta-lactam + macrolide (ex: Ceftriaxone + Azithromycin)
OR
Fluoroquinolone (ex: Moxifloxacin)
Reg respiratory settings on a ventilator, what 2 things should you think of changing when oxygenation is a problem? Ventilation?
Oxygenation is a problem—> consider changing FiO2 or PEEP (the percent oxygen in the air you are giving to the person or the positive end expiratory pressure to keep the alveoli from collapsing)
Ventilation is a problem—> consider changing Tv (tidal volume) (mL of air the patient is getting in/out) or the RR (respiratory rate) (how fast they are breathing/ blowing off CO2)
Patient has been taking Naproxen (Aleve) for years to manage chronic back pain. Labs show her kidney function is getting worse. What is the cause of her renal failure?
Analgesic nephropathy (too many NSAIDs damaged the kidneys) -most often—> Tubulointerstitial nephritis or Papillary necrosis
*Naproxen (Aleve)= NSAID
Remember that NSAIDs block PG’s (PG’s dilate the afferent)—> constriction of afferent—> decreased GFR and RPF (decrease blood flow to kidneys/ put more pressure on the kidneys)
**chronic NSAID use also can cause premature aging, atherosclerotic valvular disease, and urinary tract cancer
If you suspect a chest pain patient may have aortic dissection, should you give them aspirin?
NO! Aspirin is an antiplatelet agent-> stops clotting, and therefore causes bleeding, which would worsen aortic dissection. In fact, aspirin can kill a patient with aortic dissection.
Mechanism of action of Aspirin (ASA)?
Blocks COX-1 (and COX-2)—> decreased production of TXA2 (thromboxane A2) (*and PGs) within platelets—> decreased platelet aggregation
(It is an NSAID/ antiplatelet agent that stops platelets from sticking)
What should you give chest pain patients with possible ACS (acute coronary syndrome) (and low risk for aortic dissection) ASAP?
Aspirin
Blocks COX-1-> TXA2-> platelet aggregation
Guy has fatigue, lower extremity edema, dark urine. U/A shows protein and blood in the urine. Kidney biopsy shows dense deposits in the glomerular BM. Immunofluorescene is positive for C3, not Ig’s. Diagnosis?
Membranoproliferative glomerulonephritis (nephrotic syndrome)
*complement gets activated/ used up—> decreased C3 protein
FEV1/FVC ratio in restrictive vs obstructive lung dz?
Restrictive= problem getting air IN
FEV1 low/ FVC low= NORMAL or HIGH (less air in means less air out)
Obstructive= problem getting air OUT
FEV1 lower/ FVC low= LOW
*remember FEV1= max air you can blow out in 1 second; FVC= max air you can blow out after max inspiration
Middle aged guy has SOB on exertion. CXR shows mediastinal fullness and scattered reticular opacities in the upper lungs. Labs show calcium is high. Diagnosis?
Sarcoidosis-associated lung disease (restrictive pattern, so problem breathing in)
*Clues: he’s young, “mediastinal fullness and scattered reticular opacities”= hilar lymphadenopathy, hypercalcemia (vit D conversion by lung macrophages)
Are the following values high, low, or normal in sarcoidosis-associated lung disease?
FEV1
TLC (total lung capacity)
DLCO (diffusion capacity for carbon monoxide)
Restrictive= problem breathing in (less air in= less air out)
FEV1 (max air you can breathe out in 1 sec)= normal to low
TLC= low (problem breathing in, so lungs hold less air)
DLCO= low (inflammation and scarring interfere with gas exchange)
In ARDS, would you want to put the patient on high or low tidal volume (Vt) ventilator support?
Low tidal volume ventilation (LTVV)
-to prevent overdistention of alveoli
Lady who recently underwent chemo presents with right-sided severe abdominal pain that is constantly burning. No other symptoms, but when you touch the area it hurts a lot and no NSAIDs or antacids have helped. Likely diagnosis?
Herpes Zoster (Shingles)
*The pain can come before the vesicular rash by several days!
Patient with surgical history of gastrectomy presents with fatigue and SOB on exertion. He has a shiny tongue, low Hb, high LDH. Diagnosis?
Vitamin B12 deficiency
- gastrectomy (surgical removal of part or all of the stomach)—> loss of intrinsic factor, which is needed to absorb vit B12–> vit B12 deficiency, which is a macrocytic anemia
- why hemolysis (inc LDH)? Vit B12 is needed for DNA synthesis. If it is deficient, you get ineffective erythropoiesis (making of RBCs in the bone marrow)-> intramedullary hemolysis
Lady is having difficulty swallowing solid foods (not liquids). Lost weight, has oral thrush, dental caries, and firm submandibular nodules. Only 1 sexual partner. Next step to diagnose?
Get antibodies to Ro/SSA and La/SSB
- this sounds like Sjogren syndrome (autoimmune disorder of exocrine glands)—> dry mouth (leading to difficulty swallowing, thrush, and dental carries)
- to diagnose you need (1) evidence of dry mouth/ eyes (positive Schirmer test for decreased lacrimation) and (2) histologic evidence of lymphocytic infiltration of the salivary glands OR serum antibodies against SSA (Ro) and/or SSB (La)
Old guy with hx of metastatic squamous cell cancer has had low back pain for 2 months. In the last 2 weeks, he’s had progressive leg weakness and dribbling of urine. He has decreased strength and sensation in the lower extremities. Diagnosis?
Cauda equina syndrome
- compression of 2+ spinal nerve roots in the lumbar cistern (in his case, likely due to a tumor *other cases: large lumbar disc herniation or abscess in the region)
- the urinary incontinence is due to damage to S3-S5 (can also get sexual dysfunction)
- get an urgent MRI of the lumbosacral spine
- emergency surgical decompression within 1-2 days is required to prevent irreversible neuro damage
Most common cause of primary adrenal insufficiency in developed countries (US)?
Autoimmune adrenalitis (autoantibodies against the adrenal gland)
If you suspect lupus, what antibody should you check first?
ANA (antinuclear antibody)
-this is sensitive, so it is the best screening test. Anti-dsDNA and anti-Sm (smith) antibodies are specific, so they are confirmatory tests.
What disease do you associate each of the following antibodies with?
- Anti-cyclic citrullinated peptide
- Anti-histone
- Anti-neutrophil cytoplasmic (ANCA)
- Anti-Ro/SSA
- Anti-Scl-70 (anti-topoisomerase)
- Anti-cyclic citrullinated peptide—> Rheumatoid arthritis
- Anti-histone—> drug-induced lupus (from hydralazine, procainamide, etc.)
- Anti-neutrophil cytoplasmic (ANCA)—> vasculitis
- Anti-Ro/SSA—> Sjogren syndrome
- Anti-Scl-70 (anti-topoisomerase)—> scleroderma (systemic sclerosis)
What is serositis?
Inflammation of the serous membranes in the body (for example, the pleural lining of the lungs or the pericardium lining of the heart)
- can cause positional chest pain and SOB
- if this is part of the presentation along with fatigue, polyarthritis, etc. you would suspect lupus (SLE)
When/ how often should you do colonoscopy screening for patients with Ulcerative Colitis?
8 years after initial diagnosis and every 1-2 years thereafter
Initial treatment of frostbite?
Rapid rewarding with warm water (37-39C/ 98.6-102.2F)
*also give pain meds (rewarming tissue is painful)
*frostbite= freezing of tissue-> disruption of cell membranes, ischemia, vascular thrombosis, inflammatory changes (usually involves face, ears, distal limbs)
**do NOT do hot air rewarming (not good enough control over the temp) or rewarm by placing the limb near your abdomen in the field if there’s the possibility of refreezing before getting definitive care (freezing-> warm-> freezing can cause more damage than just freezing-> warm)
Lady twisted her ankle a month ago. The swelling improved, then got worse over the last couple weeks. Her foot, ankle, and calf are really painful now all the time. There is erythema, warmth, edema up to the calf and imaging shows patchy area of osteopenia. Diagnosis?
Complex regional pain syndrome
- can happen 4-6 wks post-trauma due to inflammatory cytokine effects
- causes burning/ tingling pain out of proportion to the injury
- associated with erythema, edema, skin changes, X-ray may show patchy demineralization
Lady on OCPs explains she has been having severe migraines with aura. What should you tell her to do?
Give off the OCPs!
Women with migraines, esp with aura, are at increased risk for ischemic stroke. OCPs (and other estrogen-containing contraceptives) increase risk for stroke too. So you don’t want to have both these stroke risk factors at once! OCPs are contraindicated in migraine sufferers for this reason.
How do you treat symptomatic prolactinoma?
Dopamine agonist (Cabergoline, Bromocriptine)
*remember that dopamine puts the break on prolactin, so by giving a dopamine agonist, you are stopping prolactin (helps normalize prolactin levels and reduce tumor size)
**only do surgery (transsphenoidal resection) if the tumor is really large (>3 cm) or not responding to meds
Patient was diagnosed with adrenal insufficiency and got put on hydrocortisone. She continues to have light-headedness and salt cravings. Next step in her management?
Add fludrocortisone (a synthetic mineralcorticoid/ aldosterone)
-she is already taking hydrocortisone (a synthetic glucocorticoid/ cortisol)…since this doesn’t do much for the mineralcorticoid/ aldosterone deficiency, she gets those symptoms (hypOnatremia/ salt cravings/ light-headedness, hyperkalmeia)
Guy was wearing contact lenses for a week straight. Is having difficulty removing the contact lenses now. He woke up with eye pain and discharge. The cornea is hazy and there is sclera injection (red/ bloodshot). Diagnosis?
Contact lens associated keratitis
-usually due to Pseudomonas and serratia (gram-neg) and require removal of contacts and antibiotics emergently! (Otherwise can-> corneal perforation, scarring, permanent vision loss)
You do a CXR on a girl with a shoulder sprain and find an incidental coin-sized lesions on the upper lobe of her lung. 1st step to work it up?
Compare to a previous CXR
Most likely it’s a solitary pulmonary nodule (SPN)= benign nodule
- no further testing if it’s stable in size >2 yrs
- if it’s changed, move on to a CT and continue to rule out or rule in cancer
Patient has rash, joint pain, fatigue. Has palpable purpura, hepatosplenomegaly. Bun and Cr are elevated, complement is low, anti-HCV (hep C) and Rheumatoid factor are both positive. Diagnosis?
Mixed cryoglobulinemia
Vasculitis (from immune complexes)
- palpable purpura on legs, joint pain, liver involvement, kidney disease/ glomerulonephritis
- associated with hep C and hypocomplementemia (depleted complement levels)
What is an AV fistula (used in dialysis) and how can it cause high-output cardiac failure?
AV fistulas connect the arteries to the veins directly
Rather than the normal path: arteries-> arterioles-> capillaries-> venous system, AV fistulas directly connect arteries-> veins (blood can dump right into the venous system at the top of the arm where the fistula is placed for dialysis access). Now the lower arm isn’t getting good perfusion-> heart makes up for it by pumping harder. This constant increase in contractility (heart having to work harder)-> high-output cardiac failure.
Upper abdominal systolic-diastolic bruit indicates what?
Renal artery stenosis
**A bruit does not usually indicate AAA (abdominal aortic aneurysm)- this would be a pulsatile mass (in <50% of patients) or picked up on screening Doppler U/S.
Reduced systemic vascular resistance (SVR) means what?
Vasodilation
Most patients with AAA (abdominal aortic aneurysm) present with what symptoms?
Most are asymptomatic! (Trick Q)
Guy has CABG (coronary artery bypass grafting) and aortic valve replacement done. 2 days later gets sudden-onset weakness, chest tightness, SOB. He is hypotensive and tachy. EKG shows irregularly irregular rhythm. Diagnosis and treatment?
A-fib
Cardiovert (it is <48 hrs plus he is hemodynamically unstable)
Defibrillation vs. cardioversion?
Defibrillation= unsynchronized shock
- “drops a bomb”/ shocks at a random point in the cardiac cycle
- use for V-fib and V-tach (Rap: “defib for V-fib and pulseless V-tach. Don’t defib asystole you won’t bring em back”)
Cardioversion= SYNCHRONIZED shock (press that sync button)
- shock is given at the QRS complex (purpose is to minimize shock occurring during depolarization, which could throw the patient into V-fib)
- example: use for a-fib if unstable, onset <48 hrs, or in a young person with a structurally normal heart after anti-coagulating with Warfarin for 3 weeks and do TEE right before to make sure there’s no clots (don’t want to throw a clot with the CV-> stroke)
Lady with HTN (on Lisinopril) and OSA (on CPAP during sleep) presents with leg swelling, worse in evenings. She has pitting edema in the bilateral ankles, dilated and tortuous superficial veins, and a small ulcer noted on the left medial ankle. All pulses are normal. Diagnosis and solution?
Chronic venous insufficiency (CVI)
(Incompetent venous valves-> backflow of blood and pooling in legs)
*ankles often appear hyperpigmented, may have ulcers
Leg elevation, compression stockings, exercise
**patients who don’t respond to these conservative treatments should get venous duplex U/S to confirm the diagnosis (by retrograde venous blood flow)
What 4 drugs improve survival in patients with LV systolic HF?
- ACE inhibitors
- ARBs
- Beta-blockers
- Mineralcorticoid receptors antagonists (Spironolactone/ Eplerenone)
*also hydralazine + nitrates in African American patients
What are electrical alternans?
Varying amplitude (height) of QRS complexes
Suggests cardiac tamponade
Holosystolic murmur beast heard over the cardiac apex with radiation to the axilla
Mitral regurg
*clinical features: SOB on exertion (dec CO due to the regurg and inc LA pressure) and fatigue…can lead to a-fib (stretched LA) and HF
Man has MI of his LAD and gets a stent placed. 10 days later presents with another MI (mid sternal chest pain, diaphoresis, SOB) with ST-elevation in leads V1-V4. Cause of this?
Medication non adherence
He’s having stent thrombosis. To prevent this, patients should be on ASA + Clopidogrel (Plavix)= dual anti-platelet therapy (DAPT). Most common cause of stent thrombosis= not taking these meds as instructed.
How do you know this is stent thrombosis, not a recurrent MI? LAD= leads V1-V4 where the stent was placed! So this is far more likely.
Young guy with HTN and alcohol abuse comes into the ED with SOB for 2 days, worse last night. BP is 220/110. He has crackles, S4, and cotton-wool spots on eyes. Cr is 2.1. He is given IV furosemide + Nitroprusside with improvement of symptoms but the next day he has a seizure. Diagnosis?
Hypertensive emergency—> next day Cyanide (CN) toxicity
Really high BP + end-organ damage (CHF, renal failure, and eye signs/ symptoms)
*cotton-wool spots= white patches on retina (high pressure damages blood supply to the nerve fibers)
IV Nitroprusside is given in HTN emergency, but gives off nitric oxide and cyanide byproducts. CN toxicity= neurologic change (seizure, altered mental status, lactic acidosis, coma)
Man with CAD and HTN is brought to the ED after a suicide attempt. BP is 75/40, HR is 40 bpm. Extremities are cold and clammy. EKG shows sinus Brady with 1st degree AV block. He is given IV fluids + Atropine w/o improvement. Next thing to give him?
GLUCAGON
-Bradycardia, AV block, hypotension and wheezing suggests beta-blocker overdose
*Remember that beta-blockers dec HR (block beta-1 on heart), can cause AV block (AV node is slowing the signal from atria to ventricles too much), can cause hypotension (block beta-1, which causes renin release), and can cause wheezing (block beta-2, which bronchodilates-> bronchoconstriction)
**extremities are cold due to peripheral vasoconstriction (inc BP, dec blood flow) to shunt blood to centrally located vital organs
***also, the fact he has CAD and HTN tells you he prob was prescribed a beta-blocker and has it available to overdose on in a suicide attempt
Guy with CAD, hx of MI comes in for retrosternal chest pain and burning, worse at night (not w/ exercise). He has cough and occasional hoarseness. Resting EKG is normal. Exercise EKG shows ST depression in the inferior leads, but myocardial perfusion study shows no evidence of stress-induced ischemia. Treatment?
PPI (like Omeprazole)
-this is GERD
- GERD symptoms mimic angina, worse at night bc acid can reflux easier when laying down
- cough and hoarseness from laryngeal irritation (from the acid)
*Although the exercise EKG shows ST depression (subendocardial ischemia), evidence of ischemia when exercising at 90% of maximal HR is NOT unusual in patients with known CAD
In terms of the EKG, how is uremic pericarditis different from other etiologies of pericarditis?
Does not typically cause diffuse ST elevation (or PR depression)
- this is bc the inflammation doesn’t affect the myocardium
- *uremic pericarditis presents in patients with advanced renal failure requiring dialysis (they come in with pleuritic chest pain and pericardial friction rub)
What is the CHADS-VASC score? What do each of the letters stand for and how do you interpret the results?
CHADS-VASC score is used to determine whether an a-fib patient should be started on lifelong anticoagulation
C- CHF H- HTN A- Age >75 (*2 points) D- DM S- Stroke/ TIA (*2 points) V- Vascular dz (prior MI, PAD, aortic plaque) A- Age 65-74 Sc- Sex (female) *everything positive counts as 1 point except age >75 and stroke count as 2 points
0–> no anticoagulation
1–> none, ASA, or oral anticoagulation
2+-> oral anticoagulation
44 year old guy with no medical hx presented with new-onset a-fib w/ RVR. Echo showed mildly dilated LA, but no valvular abnormalities. Should we have him on long-term anticoagulation, like ASA and/or Warfarin?
NO
His CHADSVASc score is 0 so it is not indicated.
C- CHF H- HTN A- Age >75 (*2 points) D- DM S- Stroke/ TIA (*2 points) V- Vascular dz (prior MI, PAD, aortic plaque) A- Age 65-74 Sc- Sex (female) *everything positive counts as 1 point except age >75 and stroke count as 2 points
0–> no anticoagulation
1–> none, ASA, or oral anticoagulation
2+-> oral anticoagulation
Pregnant lady present with SOB, S3, and holosystolic murmur at the apex. U/A shows trace protein and she has a little ankle edema. EKG shows sinus tachy. Next best step?
Echocardiogram
You need to check for peripartum cardiomyopathy (dilated cardiomyopathy that can occur during or up to 5 mo. after pregnancy). It is often associated with mitral regurg (holosystolic murmur at the apex).
Patient comes in after a car crash. Vitals are stable and physical exam is unremarkable. 30 min after arrival, his BP is 80/50 and HR is 120. Now he is having trouble breathing and has a erythematous rash and wheals over his chest and abdomen. Most likely cause?
Latex allergy (anaphylactic shock)
Fat embolism presents with what type of rash? How long does is occur after a long-bone fracture?
Petechial rash (also SOB and confusion)
12-24 hrs later! Not immediate
An aortic regurg patient is asymptomatic. How does his heart adapt to explain this?
Increased LV compliance
(The LV undergoes eccentric hypertrophy of myocardial fibers in series, meaning it stretches out/ dilates in response to the backflow of blood)
We start a patient on a statin if their ASCVD (atherosclerotic cardiovascular disease) score is what?
> 7.5-10%
Depends on the resource you’re looking at
Most common cardiac manifestation of lupus (SLE)?
Pericarditis
(*typically presents as pleuritic chest pain, pericardial friction rub, and diffuse EKG changes w/ other SLE symptoms such as joint pain)
Systolic murmur at the sternal border
Tricuspid regurg
Normal range for total bilirubin?
0.1-1.0
Alcoholic has obvious signs of cirrhosis (ascites, spider angiomas, hemorrhoids, AST:ALT >2:1). Do you need to do a liver biopsy to confirm the diagnosis of cirrhosis?
No
-though liver biopsy is the gold standard for diagnosis of cirrhosis, if the history and physical is obvious for cirrhosis, do not put the patient through this
*you also don’t need to do unnecessary work-up for rare causes of cirrhosis like alpha-1 antitrypsin deficiency or hemochromatosis. This guy is an alcoholic so you can say with confidence that the cirrhosis resulted from alcohol intake.
What screening test should you do in a patient with liver cirrhosis?
Endoscopy (EGD= EsophagoGastroDuodenoscopy)
-you need to check for esophageal varices, determine their risk for variceal hemorrhage, and come up with strategies for prevention of variceal hemorrhage (these patients bleed so much it’s life threatening!)
How do you manage acute diverticulitis (presents as LLQ pain and confirmed by CT)? Be specific about the antibiotics used. What do you need to follow up with?
Antibiotics- Ciprofloxacin + Metroniadazole (Flagyl)
And bowel rest
Follow up with colonoscopy (4-8 wks later) since colon cancer can mimic the presentation and CT findings of diverticulitis!
*also advice patients to increase fiber intake and exercise and lose weight and stop eating red meats, smoking, and straining on the toilet
**Cipro is a fluoroquinolone that is broad spectrum and good for gram neg GI bugs + Metronidazole is good for anaerobic coverage
50 y.o. heavy alcoholic presents with SOB, even at rest. He has an S3 and crackles. CXR shows pulmonary venous congestion. Echo shows dilated LV and EF of 25%. He has no history of any heart problems. What is the most likely cause of his symptoms?
Alcoholic dilated cardiomyopathy
- he has evidence of systolic dysfunction in the setting of alcohol abuse. Know that dilated CM from alcohol is a dx of exclusion (he had no prior CAD or valvular heart dz and heavy alcoholism is evident)
- abstinence from alcohol should improve or normalize LV function over time
Peripheral vascular dz vs. acute arterial occlusion? What are they
Peripheral vascular dz- blood flow is reduced to a limb (same concept as angina)
Acute arterial occlusion- blood flow is cut off to a limb (same concept as MI, emergency!)
Old man ex-smoker has worsening cramping in his left leg. He has decreased pulses in the left leg and a reduced ankle-brachial index. Diagnosis and treatment?
Peripheral artery disease
Treat with smoking cessation, graduated exercise program (walk until claudicaiton/ pain from ischemia, then rest, then do 1 more cycle), atherosclerotic risk factor reduction, avoid temperature extremes, aspirin + a stain, can also give Clopidogrel, cilostazol (surgery- angioplasty or bypass grafting- if severe)
- this usually occurs with CAD/ is a manifestation of atherosclerotic cardiovascular dz (ASCVD)
- *do not confuse with acute arterial occlusion- this is an emergency where blood flow through an artery to a limb is fully cut off! Presents with 6 P’s: pain, pallor, polar (cold), paralysis, paresthesias, and pulselessness (not just reduced pulse/ blood flow…none at all!)
Patient complains of on/off epigastric abdominal pain for 1 year, worse with eating. Hb is low, MCV is >100. Diagnosis?
Autoimmune gastritis—> pernicious anemia
(Antibodies against parietal cells—> cannot absorb vit B12–> macrocytic anemia)
*look for hypochlorhydria (decreased stomach acid- since parietal cells produce acid) and elevated gastrin (gastrin stimulates parietal cells to release acid, so it will get up-regulated in response to the low acid as feedback)
Name some functions of the liver.
- Synthetic (makes stuff)
- clotting factors
- cholesterol
- proteins (ex: protein c and s, albumin) - Metabolic
- metabolism of drugs and corticosteroids (P450 system)
- detox
- breaks down estrogen - Excretory
- bile excretion
40 y.o guy has chronic diarrhea with fat in it (no pathogens or WBCs). He’s given a oral D-xylose solution. Urinary excretion of the D-xylose is low. He is treated with Rifaximin and D-xylose test is repeated but results didn’t change. Diagnosis?
He is peeing out a LOW amount of D-xylose (monosaccharide), meaning he has a mucosal reabsorption problem like celiac dz or SIBO…but it’s not SIBO since that’s treated with Rifaximin and that did not help…so it’s celiac
(problem with reabsorption due to flattened villi-> less of the monosaccharide pushed into the blood-> less filtered through the kidneys and peed out)
*patients with malabsorption due to enzyme deficiencies would have normal absorption and urinary output of D-xylose (bc their problem is with enzymes breaking polysaccharides into monosaccharides and D-xylose is already a monosaccharide)
Explain how the D-xylose test can be used to distinguish pancreatic insufficiency from mucosal causes of malabsorption (celiac dz, bacterial overgrowth, etc.).
D-xylose is a monosaccharide and gets fully absorbed into the blood.
Pancreatic insufficiency (not getting enough pancreatic enzymes into the duodenum to break down polysaccharides-> monosaccharides)—since D-xylose is already a monosaccharide it doesn’t need the help of pancreatic enzymes, so all the D-xylose gets appropriately absorbed into the blood and a normal amount is peed out
Celiac dz (flattened villi/ problem at small intestine level with pushing nutrients into the blood/ reabsorption)—so some D-xylose does NOT get reabsorbed into the blood as it should and a low amount is peed out
Mechanism of spider angiomas and palmar erythema in cirrhosis?
Both due to hyperestrinism
Liver not working to break down estrogen—> too much estrogen
Mechanism of caput medusae in cirrhosis?
Caput medusae= dilation of superficial veins on the abdominal wall DUE TO PORTAL HTN
(Backs up portal vein-> periumbilical vein)
Truck driver comes in with SOB and sharp chest pain for 10 hrs, relieved by taking shallow breaths. BP is normal, HR is tachy, RR is 30. EKG is normal. Most likely diagnosis?
PE (pulmonary embolism)
*presents with SOB, pleuritic chest pain, tachypnea, tachycardia (CXR may appear normal)
Guy with long extremities, flexible joints, and pectus carinatum has sudden-onset chest and neck pain. Diagnosis?
Aortic dissection
-this guy has Marfan syndrome (mutation of fibrillin-1-> connective tissue integrity problems throughout the body, including aortic root dilation)
20 y.o guy is having depression and involuntary movements. Total bili, direct bili, AST, and ALT are elevated. Diagnosis?
Wilson disease
- rare AR disease in which copper transport is impaired—> copper accumulation in tissues
- consider this when there is liver dysfunction + neuro psych symptoms!
Which has a greater impact on BP reduction: following the DASH diet or reducing sodium in your diet?
DASH diet
*the following can decrease BP by this much: Weight loss—5-20 per 10kg loss DASH diet—8-14 Exercise—4-9 Dietary sodium reduction—2-8 Limiting alcohol—2-4
**tell patients to do all of the above, but losing weight and eating a DASH diet (all-around healthy diet rich in fruits and veggies, low in saturated and total fats) is key to lowering BP, more so than limiting salt
Patient has S3 and SOB. Best initial therapy?
Loop diuretics
He has LV failure (backing up to lungs). Taking off fluid is the first step in providing symptomatic relief.
*yes, drugs like beta-blockers are helpful in the long-term and reduce mortality, but this wouldn’t be the best initial therapy—wouldn’t take the excess fluid off to make the patient feel better
What heart problem can amyloidosis cause?
Restrictive cardiomyopathy
Amyloidosis= misfolded protein that deposits around the body
Diarrhea + leukocytosis. Think of what?
C diff
What is SBP?
Spontaneous bacterial peritonitis
-infection of the ascitic fluid
- presents as abdominal discomfort in a cirrhosis patient, possibly mental status change
- diagnose by PMN (neutrophil) count >250 + positive peritoneal fluid culture
Woman with SLE on Prednisone comes in for fever, chills, fatigue, cough, and SOB. Pulse ox is 86% and she’s using accessory muscles to breathe. LDH is elevated. CXR shows bilateral interstitial infiltrates. Diagnosis?
PCP pneumonia
*it’s associated with AIDS, but also immunosuppressed people (she’s taking glucocorticoids/ steroids, which block the immune system)
Patient has burning chest pain for 2 hrs. Lungs sound clear. EKG shows ST elevation in leads II, III, and aVF. You give him nitroglycerin. A few minutes later, he’s lightheaded and his BP dropped from normal to 75/50. What happened? Next step?
ST elevation in II, III, aVF= inferior STEMI (occlusion of the RCA). Inferior wall MI’s have a 50% chance of involving the RV. Since he has clear lungs (meaning left heart is good), it probably did involve the right heart.
In a right sided MI, you don’t give nitrates bc the right heart is preload dependent and this will drop BP too much!
Since you already gave nitros and his BP did drop too much, give a normal saline bolus (IV fluids) to get the preload back up (which will improve CO and BP).
Normal CD4+ count?
> 500 (*10^6/ L)
Does it help if alcoholic cirrhosis patients stop drinking?
Yes! Alcoholic cirrhosis-> liver inflammation after drinking involving fibrosis and nodule formation. This fibrogenesis improves with abstinence from alcohol.
Although advanced cirrhosis is irreversible, avoiding alcohol still carries a huge survival benefit.
How does disseminated MAC (mycobacterium avium complex) infection present?
Constitutional (fever, night sweats, fatigue, malaise, weight loss) and GI (diarrhea, abdominal pain) symptoms
Normal AST? Normal ALT?
8-40 is the normal range for both AST and ALT
Obese patient has high AST of 80 and high ALT of 90 + mild hepatomegaly. Not an alcoholic. No other signs/ symptoms. Diagnosis?
Nonalcoholic fatty liver disease (NAFLD)
- we see a mild elevation in liver enzymes in these patients (AST/ALT ratio <1) and mild hepatomegaly. Alk phos may also be on the high side. Albumin and bili are typically normal.
- diagnose by labs and U/S showing hyperechoic texture of the liver (liver biopsy would confirm but we don’t do this for fatty liver)
- treat with weight loss/ manage metabolic risk factors
Regarding class I antiarrhythmic drugs, what is “use dependence?”
Class I anti-arrhythmic drugs block Na+ channels in depolarization (phase 0)
In patients with faster heart rates, the drug has less time to dissociate from the Na+ channels—> longer effect of the drug (more widening of the QRS interval/ ventricular contraction)
**this is why class I anti arrhythmic drugs (esp class IC) are good at treating supraventricular tachyarrhythmias
What happens to SVR (systemic vascular resistance) and afterload in HF?
SVR goes up (vasoconstriction)
Afterload goes up
*Here’s the cycle of hemodynamics in HF:
Dec contractility-> dec CO-> poor perfusion to kidneys activates RAAS-> vasoconstriction (inc SVR)-> inc afterload (the vasoconstriction/ inc BP increases the pressure the heart now has to pump against)-> decreases the contractility even more since the extra afterload makes it harder to pump…so its a nasty cycle
Why might a HF patient have mitral regurg (holosystolic murmur at the cardiac apex)?
LV dilation (due to decreased CO)/ remodeling—> functional mitral regurg
What is cardiac index?
Basically the same as cardiac output, but takes into account the person’s body weight
*Cardiac Index (CI)= CO/ body surface area
Septic shock and anaphylactic shock both fall under what category of shock?
Distributive shock
“Warm shock” from vasodilation
Most common cause of mitral regurg?
Mitral valve prolapse (MVP)
Myxomatous degeneration of the mitral valve
Patient with known HFrEF on ASA, Digoxin, Lasix, Metoprolol, Lisinopril, and Atorvostatin presents with worsening SOB and lower extremity edema. You give her IV Lasix and edema improves but a few days later she has a few beats of wide complex V-tach. Next step?
Check serum electrolytes!
If a patient is stable in V-tach, you need to find out why there are having this arrhythmia (if unstable defibrillate)! She likely has electrolyte imbalance due to the IV Lasix/ Fuorosemide, which is a loop diuretic and causes hypokalemia and hypomagnesemia. Low K+ and Mg can lad to V-tach. If this is the case, you need to correct her electrolytes.
What is another name for vasospastic angina?
Variant angina or Prinzmetal angina
Mechanism and treatment for Vasospastic/ Variant/ Prinzmetal angina?
Mechanism= the intima layer of the artery smooth muscle is hyperactive—> intermittent coronary artery vasospasm (ST elevation during chest pain episodes lasting <15 min)
Treatment= CCB’s (Diltiazem, Amlodipine)
- cause coronary artery vasodilation to prevent vasospasm
- Nitrates given to stop chest pain during an episode
Guy comes in with sudden-onset severe left-sided chest pain. Has HR of 125, BP of 160/90, ST depression and T-wave inversion in leads V4-V6. He is agitated, pupils are dilated, and nasal mucosa is atrophic. What should you give him?
IV Benzo (like Diazepam)
This guy is on cocaine (tachy, HTN, signs of MI specifically NSTEMI, dilated pupils, nose jacked up from snorting cocaine) having cocaine-induced MI.
Benzos bind to GABA and enhance its inhibitory CNS activity-> less sympathetic activity so reduced agitation, improved HR and BP, improvement in cardiac symptoms.
*also give ASA (antiplatelet to stop thrombus formation enhanced by cocaine), nitrates, and CCBs to vasodilate. Do NOT give beta-blockers due to unopposed alpha-1 constriction-> worsening vasoconstriction!!
- *Remember cocaine blocks NET and DAT (NE and dopamine reuptake)-> inc NE and dopamine in the cleft. NE= alpha-1> beta-1 agonist, so causes vasoconstriction (including coronary vasoconstriction).
- *Use alpha-blockers in cocaine toxicity where BP is super high
Patient is found to have premature atrial complexes (PACs) on EKG. Is not symptomatic. Drinks 1-2 beers/ day. Best way to manage this patient?
Advise quitting alcohol
PACs are early beats from the atria firing on its own, you see early P waves (QRS is normal bc conduction below the atria is normal). Usually asymptomatic and does not require treatment, however advice to quit tobacco, alcohol, caffeine, stress bc these things can be what’s causing it!
*if symptomatic (palpitations) a beta-blocker can be given
Old guy comes into the ED with the worst pain in his life in his chest and back. He has a diastolic decrescendo murmur at the sternal border and is tachy. Has nonspecific ST-segment elevation and T-wave changes. CXR shows widening of the mediastinum. Diagnosis?
Acute Aortic Dissection
*Diastolic murmur at sternal border= aortic regurg (dissection can pull apart at aortic valve)
What fasting blood glucose and hemoglobin A1c do you need to meet criteria for a diagnosis of diabetes?
Fasting blood glucose >125
Hb A1c of 6.5% or more
For patients <40 yo with ASCVD or >40 yo with DM, what med do you give?
A statin! (Long-term)
Asthma patient in respiratory distress is given nebulized albuterol, IV methylprednisolone, and supplemental O2. Repeat labs show leukocytosis (high WBCs). Why?
Glucocorticoids (methylprednisolone) cause mobilization of marinated neutrophils-> inc WBCs
(Medication effect)
What are the 4 severity levels of asthma? State the frequency of symptoms (times they need to use SABA albuterol rescue inhaler) for each.
- Intermittent- symptoms 2 or less days/ week (treatment= SABA prn)
- Mild persistent- symptoms >2 days/ week but not daily (SABA prn + low-dose ICS)
- Moderate persistent- symptoms daily (SABA prn + low-dose ICS + LABA (or medium-dose ICS))
- Severe persistent- symptoms throughout the day (SABA prn + medium-dose ICS + LABA)
* if worse: SABA prn + high-dose ICS + LABA + oral corticosteroid and/or Omalizumab (if allergies too)
Smoker guy is planning to get a knee replacement surgery in a month. He has COPD and HTN. What will decrease his risk of post-operative pulmonary complications the most?
Quitting smoking right now
There is no evidence that drugs (such as Moxifloxacin) or anything else decreases PNA risk in the setting of surgery. There is, however, evidence that quitting smoking 1-2 months prior to surgery decreases post-op pulmonary risk by a lot!
What valvular issue can cause hemoptysis?
Mitral stenosis
(Mitral valve has a hard time opening-> blood backs up to LA and lungs-> pulmonary edema and that extra pressure in the lungs can burst capillaries-> cough up blood)
Another name for bronchogenic carcinoma?
Lung cancer!
Most common cause of hemoptysis?
Pulmonary airway disease
(Chronic bronchitis, bronchiectasis, lung CA)
-Chronic bronchitis (the constant coughing and irritation from mucus plugs can cause bursting of blood vessels in the bronchus), Bronchiectasis (same reason- you also have chronic coughing and mucus trapping from the abnormal dilation of the bronchus), and Bronchogenic carcinoma/ Lung cancer (likely due to coughing and maybe related to the rich vascular supply of the tumor)
Asthma patient comes in with worsened SOB and cough (asthma attack). Pulse ox= 88%. Patient is wheezing and using accessory muscles to breathe. ABG shows: pH of 7.43, PaO2 of 65, PaCO2 of 40. CXR shows hyperinflated lungs. What is most concerning and indicates the patient is getting worse?
Most concerning= the fact that PaCO2 is normal-high
- Why? The normal response to an asthma exacerbation is hyperventilation (compensation for not breathing well)—> blowing off more CO2–> low PaCO2 (<40). If you are not hyperventilating in an asthma attack, you are not blowing off as much CO2 and PaCO2 will be high >40–this suggests respiratory muscle fatigue or severe air trapping suggesting RESPIRATORY COLLAPSE.
- CXR showing hyperinflation is expected in an asthma exacerbation (obstructive= hard to breathe out= air trapping)
Patient with PMH of leukemia who got stem cell transplantation and developed neutropenia presents with fever, pleuritic chest pain, hemoptysis. CXR shows right upper lobe infiltrate. CT of chest shows nodular lesions surrounded by ground-glass opacities in the right upper lobe. Sputum gram stain shows inflammatory cells but no organisms. Diagnosis and treatment?
Invasive aspergillosis
(Fever, pleuritic chest pain, and hemoptysis in immunocompromised)
Voriconazole + an echinocandin (Caspofungin)
Most common cause of Cor-pulmonale in the US?
COPD (accounts for 25% of cases)
(Widespread vasoconstriction in pulmonary vasculature to shunt blood to areas where there’s better oxygen…but problem is all areas are diseased, so this just creates a greater pressure that the right heart has to pump against-> right-sided HF)
HIV patient off his meds presents with fever, cough, SOB. Has bilateral lung crackles. CXR shows bilateral interstitial infiltrates. Patient is given antibiotics and IV NS (normal saline) at 150mL/hr. 2 days later his SOB improved but he is confused and Na+ levels are lower than on admission. Cause of his hypOnatremia?
SIADH
- He has PCP pneumonia (HIV, classic fever + cough + SOB symptoms, crackles, CXR infiltrates)
- SIADH can happen from PNA= too much retention of water-> low sodium concentration
- Giving normal saline will worsen this kind of hypOnatremia (although it’s salty and you’re giving back some Na+, it is FLUID and that fluid dilutes the [Na+] more)
When you suspect lung CA what should you do?
CT of the chest
How can cirrhosis cause lower extremity edema?
Bad liver—> not making albumin like it should—> low oncotic pressure holding fluid in vessels—> peripheral edema
What is Spontaneous bacterial peritonitis (SBP)?
An infection of the ascitic fluid
*usually occurs in patients with underlying chronic liver disease and ascites. Spontaneous bacterial peritonitis (SBP) is often associated with fever and abdominal pain (can also present with hepatic encephalopathy alone)
What does “serial” mean in medicine?
Repeat
For example, “serial troponin” means you are measuring troponin several time (usually q8 hrs). “Serial CT scan” for lung cancer screening means you are doing a CT annually.
What is empyema?
Collection/ pocket of pus in the pleural space
- empyema often results from untreated exudative pleural effusion (usually secondary to bacterial PNA)
- give antibiotics and do aggressive draining of the pleura with thoracentesis. If that doesn’t do it, do throacotomy (surgical opening up of the chest to gain access to the pleural space/ open drainage)
Renal failure= GFR of less than what?
GFR <30 mL/min
You have a patient that needs to be started on anticoagulation (for PE, for example). The patient has a GFR of 20mL/min. Which initial anticoagulation med is best and why? A) Enoxaparin B) Fondaparinux C) RivaroXaBAN D) Unfractionated heparin E) Warfarin
D) Unfractionated heparin
A) Enoxaparin= low-molecular-weight heparin (LMWH)
B) Fondaparinux= IV factor Xa inhibitor
C) RivaroXaBAN= oral factor Xa inhibitor
E) Warfarin
Cannot use A, B, C, E^ because the patient has renal failure (GFR <30) and these anticoagulants are not recommended for patients with renal insufficiency (takes too long to clear them-> increased factor X activity and bleeding risk)
*Remember that LMWH (IV) is the best choice for renal insufficient patients and bridge to Warfarin (PO)!
Small cell lung cancer patient has SIADH (paraneoplastic syndrome) causing hypOnatremia. What’s the best initial treatment for the patient’s hypOnatremia?
Fluid restriction
SIADH-> too much ADH-> too much retention of fluid diluting [Na+] so that it is low
Less fluid will help this concentration come back up
*SIADH drugs (Vaptans and Demeclocycline) can be used to block V2 ADH receptors, but start with fluid restriction and see if that is enough
Most common side effect of Beclomethasone?
Most common side effect of inhaled corticosteroids (ICS) like Beclomethasone (in asthma, COPD)= OROPHARYNGEAL THRUSH (oral candidiasis)
Patient takes the following meds at home: Aspirin, Diltiazem, Atorvostatin, and Albuterol as needed. Was recently diagnosed with stable angina and recently had a nasal polyp removed. Present with SOB and wheezing. Diagnosis?
Aspirin-exacerbated respiratory distress (AERD)
*ASA and all NSAIDs block COX—> more shunting toward LOX in AA pathway—> more leukotriene synthesis, which causes bronchoconstriction and can bring on an asthma attack
What is a parapneumonic effusion?
A pleural effusion that arises as a result of a pneumonia
*subtypes: uncomplicated, complicated, and empyema
Light’s criteria?
P:S (pleural: serum ratios)—
Protein >0.5
LDH >0.6
Pleural LDH > 2/3rds the upper limit of normal for serum LDH
If any of these are true, it is exudative (“extra shit in it”) vs. transudative (fluid only)
What are the 3 types of Aspergillus infections and their presentations?
- Allergic Bronchopulmonary Aspergillosus (ABPA)
- Pulm infiltrates, wheezing, IgE in an asthma or CF patient - Aspergilloma (fungal ball)
- Gravity-dependent lung cavitation, fever, hemoptysis in a patient with prior TB - Invasive pulmonary Aspergliosis
- Fever, hemoptysis, chest pain, SOB-> kidney failure, endocarditis, ring-enhancing lesions in brain, and sinus tissue necrosis in an immunocomprimised/ neutropenic patient
How do you diagnose Aspergilloma?
Will present as a lung cavitation in a patient with prior TB (seen on chest CT) and you get Aspergillus IgG serology to confirm
Does lung compliance increase or decrease in ARDS?
Decreased lung compliance
-ARDS= inflammatory condition in the setting of infection (sepsis, PNA, etc.), trauma, or other conditions (pancreatitis, massive transfusion). Lung injury causes the release of proteins, inflammatory cytokines, and neutrophils into the alveolar space (hyaline membranes). This leads to leakage of bloody and proteinaceous fluid into the alveoli, alveolar collapse due to loss of surfactant, and DIFFUSE ALVEOLAR DAMAGE-> inability to expand/ stiff lungs/ dec compliance
What happens to the ratio of arterial oxygen tension to fraction of inspired oxygen in ARDS?
It decreases
Arterial oxygen (PaO2) to fraction of inspired oxygen (FiO2) ratio: PaO2/ FiO2 (also called P/F ratio) Decreases (<300) bc the lung injury/ hyaline membranes impair gas exchange-> decreases PaO2 and raises the FiO2 requirement (the oxygen that you have to give them through the ventilator)
70 y.o. man has a history of attacks of dyspnea on exertion. He has an ejection-type systolic murmur along the left sternal border that decreases with squatting. What does he have?
HOCM
- remember that HOCM is a SYSTOLIC murmur at the left sternal border (systolic bc the problem is when the blood is being pumped out through the aorta)
- remember that squatting increases preload (compress leg veins= more ‘milking’ of blood to heart), which makes the problem better (more blood to push septal defect out of the way)
Inheritance pattern of HOCM?
Autosomal dominant
*caused by mutations in sarcomere genes (ex: cardiac myosin binding protein C and cardiac beta-myosin heavy chain gene) for the myocardial contractile proteins of the heart
If you suspect aortic dissection, what imaging do you do?
TEE (trans esophageal echocardiogram) is preferred
But you can also do a chest CT with contrast (if patient’s kidneys are ok/ can tolerate contrast) or an MRI (if non-emergency and patient can lie still)
*do whichever of these is available at the time
What is the recommendation for AAA screening?
Abdominal ultrasound once on men 65+ who EVER smoked
What is the recommendation for breast cancer screening?
Mammogram every 2 years on women 50-74
What is the recommendation for cervical cancer screening?
Pap smear every 3 years on women 21-65
*women 30-65 may substitute w/ HPV testing every 5 yrs
What is the recommendation for colon cancer screening?
Fecal occult blood test (FOBT) or fecal immunochemical test (FIT) every year
OR
Colonoscopy every 10 years
What is the recommendation for HIV screening?
Do HIV antibody screen once in adults 15-65
What is the recommendation for lung cancer screening?
Low-dose CT scan every year in adults 55-80, 30+ pack-years of smoking, current smoker, or quit in last 15 years
What is the recommendation for osteoporosis screening?
DEXA scan in women 65+
Patient presents with worsening SOB, pitting edema in legs, hepatojugular reflux. Has a pleural effusion—what is it most likely due to?
CHF
-CHF—> increased hydrostatic pressure pushing fluid out of vessels—> transudative pleural effusion
*you’d expect: Pleural protein: serum ratios to be... Protein <0.5 LDH <0.6 LDH < upper 2/3rds limit of normal serum
A glucose of <60 (or pleural: serum glucose ratio of <0.5) represents what type of pleural effusion?
Complicated parapneumonic effusion (exudative pleural effusion in the setting of pneumonia)
Criteria for extubation (of a person on a ventilator)?
- pH > 7.25
- Adequate oxygen on minimal support (FiO2 less than or equal to 40%, PEEP less then or equal to 5)
- Intact inspiratory effort and sufficient mental alertness to protect the airway
* if a patient is ready to be exubated based on the above criteria, do a spontaneous breathing trial (keep them intubated but turn off ventilator support to check that they breathe on their own and ABG remains normal throughout this effort)!
Symptoms of CHF + peeing out protein. Think about what?
Cardiac amyloidosis (Amyloid, a misfolded protein, deposits in various tissues, including the heart-> restrictive CM and you pee out some excess protein)
Patient has sharp chest pain worse with deep breathing, better with leaning forward. BUN and Cr are elevated a lot. Diagnosis and treatment?
Uremic pericarditis
(Toxins accumulate and cause inflammation of the heart sac)
Hemodialysis
How does acute HIV infection present?
Mono-like symptoms (fever, lymphadenopathy, sore throat, athralgias) 2-4 weeks post-exposure
*Viral load is really high (>10,000 copies/mL) (but HIV antibody testing may be negative adn CD4 still normal)
Patient has fatigue, SOB on exertion, lower extremity edema, proteinuria, easy bruising. Echo shows concentric thickening of ventricular walls w/ diastolic dysfunction. Diagnosis?
Amyloidosis
- Causes a restrictive CM + peeing out protein
- Remember, it’s a misfolded protein that deposits in various places (systemic dz)
What is dumping syndrome?
Seen in gastric bypass patients
The stomach is now so small that food, esp simple carbs, gets dumped into the intestines really fast-> diarrhea (can also cause abdominal pain, nausea, hypotension, tachycardia, lightheadedness)
Mechanism of vasovagal syncope?
Severe dehydration, etc.-> dec preload to heart-> dec CO-> cardiopulmonary receptors recognize there’s less volume in the heart-> initially this causes inc sympathetic activity, so inc HR and contractility to raise CO to normal-> contortion/ weird twisting of the LV (bc it’s pumping normal but there’s not enough blood to pump out)-> messes up cardiopulmonary receptors so that they have the opposite effect (they think the heart is over full)-> dec sympathetic activity, so dec HR and contractility-> lack of blood to brain-> body faints to inc preload back again (gravity isn’t against you when you’re laying on the floor)
What is a pericardial knock and when do you hear it?
Mid-diastolic sound associated with constrictive pericarditis
Remember, constrictive pericarditis= fibrotic, scarred pericarditis (from repeated inflammation/ recurrent pericarditis). This restricts diastolic filling of the heart-> “pericardial knock” during diastole.
What screening do you need to do for cirrhosis patients?
EGD (endoscopy) to screen for esophageal varices
What med can you give for esophageal varices?
Non-selective beta blocker (Propranolol or Nadolol)
-Block beta-2 (vasodilates)-> vasoconstricts-> reduces portal blood flow
Would you expect PT and albumin to be high or low in a cirrhosis patient?
PT- High (liver makes clotting factors. If the liver is bad, it’s not making as many clotting factors and PT goes up bc takes longer to clot)
Albumin- Low (liver makes albumin. If the liver is bad, makes less of it)
Besides in B12 and folate deficient individuals, we see macrocytic anemia in what population of patients?
Alcoholics
Explain high-output cardiac failure in a hemodialysis patient with an AV fistula.
AV fistula= direct connection between artery and vein (blood goes in arteries away from heart and meets up right away with vein back to heart rather than having to journey through tiny vessels first)
Way more blood in venous system to heart—> heart has to deal with more blood, so a preload overload—> high-output cardiac failure
*these patients get a wide pulse pressure (ex: 160/90) bc in systole the heart pumps out a huge amount of blood (due to having more preload) and during diastole blood is shunting across the AV fistula to VEINS so the pressure drops a lot in the ARTERIES
Patient had penetrating injury to right eye which resulted in blindness in the right eye. 2 weeks later presents with “floating spots” and blurry vision in his left eye. Most likely cause?
“Spared eye injury”
Damage to eye-> exposes antigens your body has never seen (‘hidden antigens’)-> immune system responds to them and attacks other eye
Guy presents with SOB, cough, hemoptysis for 2 days. He has had weight loss and rhinosinusitis. Labs show low Hb, high BUN and Cr, high WBCs. CXR shows lung nodules. Diagnosis?
Granulomatosis with polyangiitis (Wegner’s)
-systemic vasculitis that involves nasopharynx + lungs + kidneys
Patient flexes his right hip and knee and slaps his foot to the floor with each step. What gait is this?
“Steppage gait”
L5 radiculopahty adn compression peroneal neuropathy are common causes
Lady had a liver transplant 2 weeks ago (is on immunosuppressant meds). Has fever, chills, weakness, vomiting. Fever, low BP, tachy. Most likely cause of her presentation?
Bacterial infection
- most infections within the first month are bacterial causes, during months 1-6 opportunistic (in setting of immunosuppression)
- hemodynamic instability (look at the vital signs) makes bacterial infection more likely than transplant rejection
What med can treat an actively bleeding esophageal varices?
Octreotide
Lady comes in with periorbital edema and proteinuria. She is started on diuretics and the edema improves. Then she gets severe right-sided abdominal pain, fever, and gross hematuria. Why?
Renal vein thrombosis
Remember that nephrotic syndrome (esp membranous GN)-> peeing out protein, including antithrombin III-> hypercoagulable state
60 year old man has diarrhea w/ blood and mucus. Has not been on antibiotics. Colonoscopy 4 years ago was normal. Has elevated WBC count and ESR, low Hb. Sigmoidoscopy shows erythematous friable mucosa from the rectum to sigmoid colon. Diagnosis?
Ulcerative colitis (UC)
*has a bimodal distribution- more common in young (15-40) and old (50-80)
**NOT colon cancer…although low Hb in elderly is colon cancer until proven otherwise, the colonoscopy 4 years ago did prove otherwise (only need 1 every 10 years). Plus, the sigmoidoscopy showing involvement of just the distal colon is constituent with UC (bleeding-> low Hb from that)
Patient has coffee ground emesis + black, tarry stools. What are you thinking?
Upper GI bleed
*look for elevated BUN (due to increased GI digestion/ breakdown of Hb)
Lady with osteoarthritis (takes NSAIDs) has conjunctival pallor. Most likely cause of her anemia?
Iron deficiency anemia from NSAIDs (block GI protective prostaglandins-> gastritis and/or gastric ulcers leading to chronic GI blood loss and depletion of iron stores)
*osteoarthritis does NOT cause anemia of chronic dz!
Patient with BMI of 55 and extensive smoking history has SOB, clear lungs, distant heart sounds, low-voltage QRS complexes on EKG, Hb 16, pH 7.3, PaCO2 60. Diagnosis?
Obesity hypoventilation syndrome
- BMI >30 (obese)
- Lungs are clear
- Distant heart sounds and low-voltage QRS= heart is further away due to excess fat in between (*think of this and pericardial effusion)
- Reactive polycythemia (poor oxygenation due to shallow breaths-> kidneys inc EPO-> inc Hb to try to compensate by having more O2 binding sites)
- Respiratory acidosis (retained CO2 from shallow breathing)
In a patient with poor oxygenation, why might you see inc Hb?
Reactive polycythemia
Poor oxygenation-> kidneys pump out more EPO-> more Hb to try to compensate by providing more oxygen binding sites
3 diagnostic criteria for obesity hypoventilation syndrome?
- Obesity with BMI >30
- Daytime hypercapnia (PaCO2>45)
- No alternate explanation of their hypoventilation
- work it up by getting ABG (hypercapnia, normal A-a gradient), r/o pulm disease w/ CXR, restrictive pattern on PFTs (all the fat restricts them from expanding their lungs), normal TSH, polysomnography
- treat with weight loss/ bariatric surgery, nocturnal positive-pressure ventilation
- *most of these patients have coexisting OSA
Patient with cardiomyopathy is on Furosemide (Lasix), Carvedilol, Lisinopril, and Digoxin. She presents with a-fib w/ RVR and you treat her with RivaroXaBAN and Amiodarone. 2 weeks later, she comes back with anorexia, nausea, weakness. Why?
Digoxin toxicity (causes GI symptoms)
She was already taking Digoxin. You added Amiodarone (anti-arrhythmic) to her regime, which blocks the P450 system (broken chrome bumper in uno, does, tres sketchy)-> inc Digoxin in blood.
Normal leukocyte (WBC) count?
4,500-11,000
*just remember it as roughly <10,000
What is Myasthenia Gravis and how do meds like Pyridostigmine work for it?
MG= antibodies against the nicotinic ACh receptors on the post-synaptic at the motor end plate (skeletal muscle NMJ)-> proximal muscle weakness worse w/ use, ptosis, diplopia
Pyridostigmine= ACh-esterase inhibitor-> blocks the breakdown of ACh-> more ACh in the cleft to outcompete MG antibodies
What is a Myasthenic crisis?
Exacerbation of Myasthenia Gravis (antibodies going crazy against post-synaptic nicotinic ACh receptors-> muscle weakness)
- can be brought on by infection, surgery, pregnancy/ childbirth, tapering off immunosuppressant drugs, some meds (aminoglycosides, beta blockers)
- presents with oropharyngeal and general weakness, respiratory insufficiency
- intubate, plasmapheresis or IVIG + corticosteroids
Lady with Myasthenia Gravis and Hypothyroidism presents with SOB, productive cough, and choking sensation. T 101, BP 130/80, HR 110, RR 22. She takes shallow breaths and has crackles at lung bases. High WBCs, resp acidosis (low pH, high CO2). Diagnosis and next step?
Myasthenia crisis
Endotracheal intubation
- This patient has PNA (SOB, productive cough, shallow breathing, crackles, WBC count). Resp acidosis (low pH, high CO2) explained by not breathing deep-> less air getting down into lungs for gas exchange. This was a trigger for MG crisis/ exacerbation.
- Do elective intubation bc of evidence of impending respiratory failure (ill-appearing, tachypnea/ breathing rapid and shallow, muscle weakness, difficulty clearing secretions/ choking sensation, and respiratory acidosis).
We should do elective intubation in patients with evidence of impending respiratory failure. What kind of subjective and objective signs serve as evidence that they’re going to lose ability to support their airway and you should intubate?
Subjective:
- they look really sick
- tachypnea (breathing fast and shallow)
- muscle weakness
- can’t clear secretions/ choking
Objective:
- low vital capacity (after max inspiration, the max air you can exhale/ breathe out) *low means they have a weak ability to exhale
- respiratory acidosis (retaining CO2 from poor gas exchange)
You see low Na+ and high K+ in the labs. What should you automatically think of?
A problem with aldosterone!
Remember, aldosterone-> Na+ absorption, K+ and H+ wasting. If aldosterone is low, you get dec Na+ in the blood and inc K+, H+ in the blood-> hypOnatremia, hypERkalemia, and metabolic acidosis.
Normal fasting glucose?
70-110
Guy from Southeast Asia has lightheadedness, cough, unexpected weight loss. Has fever, low BP. Labs show low Na+, high K+, low glucose, eosinophilia. CXR shows airspace disease in upper lung w/ lymphadenopathy. Diagnosis?
Military TB-> infectious adrenalitis/ primary adrenal insufficiency (Addison’s disease)
- Remember, no.1 cause of Addison’s in the US= autoimmune destruction of adrenal glands. But no.1 cause of Addison’s in developing countries= TB! The inflammation from military TB destroys adrenal glands so that they stop producing hormones.
- Addison’s= adrenal glands aren’t making aldosterone and cortisol-> low Na+ in blood (low BP, weakness/ lightheadedness, hypOnatremia), high K+ in blood (hypERkalemia).
Girl is treated for asthma exacerbation with albuterol nebulization + IV methylprednisolone. Her asthma symptoms improve, but now she has severe muscle weakness and hand tremor. Next step?
Check serum electrolyte panel
Albuterol= beta-2 agonist-> hypokalemia (stimulates sodium potassium pumps, so brings K+ into cells). HypOkalmeia can cause muscle weakness and tremor.
*Another side effect is palpitations (speed up the heart bc has some agonist effects on beta-1 too)
Old lady has lethargy and SOB. Hypotension, tachycardia, reduced breath sounds and crackles. Systolic ejection murmur at right upper sternal border. High cardiac index, normal RA pressure, normal pulmonary capillary wedge pressure (LA pressure). Low SVR. What clinical picture does this fit?
Septic shock
- note: you can’t meet all the SIRS criteria based off this question, have to roll with just the info they give you. But the clinical picture is septic shock- possible PNA for infection source (crackles and SOB), hemodynamic instability (low BP, tachy), low SVR= widespread vasodilation in response to inflammatory cytokines.
- high CI (which is CO taking into account body size) and no problems with the heart, so not a cardiogenic shock picture (inc CO is the heart trying to compensate for low BP).
**do NOT get thrown off by the murmur (systolic at right upper sternal border). This is aortic stenosis- a lot of old people have it due to calcifications!
What types of shock present with cold extremities?
- Cardiogenic shock
(Heart is not pumping blood out well to extremities and vasoconstriction to divert blood to vital organs) - Hypovolemic shock (hemorrhagic shock)
(Body vasoconstricts to divert blood away from extremities and toward vital organs)
Do “bounding pulses” always indicate aortic regurg?
No
Just means the heart is working overtime (inc CO)
Usually use BiPAP or CPAP in:
- COPD exacerbation
- Obstructive Sleep Apnea
COPD exacerbation—> BiPAP
Obstructive Sleep Apnea—> CPAP
What is the goal for O2 sat in a COPD exacerbation patient?
88-92%
*if higher, you will inhibit their respiratory drive (based on low oxygen, not high CO2 like normal people since they have chronic CO2 retention and are desensitized to it)-> hypoventilation (slows or stops their breathing)
Patient is treated for COPD exacerbation. Treatment includes noninvasive ventilation (BiPAP), which is stopped. Patient has improved respiratory symptoms, but now has altered mental status. O2 sat is 96%, vitals normal. Next step?
Get an ABG (arterial blood gas analysis) to confirm acute hypercapnic respiratory failure
- remember our O2 sat goal in COPD’ers is 88-92% due to their respiratory drive being controlled by low O2 (vs. high CO2)…giving too much O2 will stop their respiratory drive to breathe
- also, too much O2 may encourage hypercapnia (CO2 retention) and worsened VQ mismatch (in COPD you have vasoconstriction in lungs to shunt blood to better oxygenated areas…if you flood in the oxygen, there will be areas that vasodilate thinking the oxygenation is good now, so blood will be sent to this damaged tissue but can’t gas exchange well so the CO2 just builds up more)
- hypercapnia (CO2 retention)-> delirium, confusion, lethargy, eventually coma and seizures
