Step Up-Ambulatory Medicine Flashcards
What are the two most common causes of hypertension?
1) Essential HTN (95%) 2) OCPs are the most common secondary cause of HTN. Other secondary causes include renovascular disease, endocrine disorders, medications, coarctation and OSA.
Why are patients with HTN at increased risk of CAD, PVD and CVA?
HTN accelerates atherosclerosis
4 non-modifiable risk factors for HTN
1) Age > 60 2) Male 3) African-American 4) FHx
3 modifiable risk factors for HTN
1) Obesity 2) Sodium intake 3) Alcohol intake > 2 oz.
Complications of uncontrolled HTN
1) Cardiovascular: MI, CHF due to LVH, PVD, aortic dissection 2) Retinopathy: AV nicking, cotton wool spots, scotomata, hemorrhages, exudates and papilledema 3) CNS: hemorrhage, TIA, CVA and lacunar stroke 4) Renal: nephrosclerosis (atherosclerosis of afferent AND efferent arterioles), decreased GFR and ESRD
Diabetic & renal disease definition of HTN
> 130/80
A patient comes in for a BP check, how long should you wait if they just drank coffee or had a cigarette?
30 minutes
A patient comes to clinic and has blood pressure elevations on two separate visits over a span > 4 weeks. You diagnose him with HTN and assess for target organ damage. What labs do you want to order at this time?
1) UA (proteinuria) 2) BMP (K, BUN, Cr) 3) FBG (r/o DM) 4) Lipid panel (minimize atherosclerosis) 5) ECG (check for LVH)
When will most newly diagnosed patients with HTN get 2-drug tx from the start?
Stage II (> 160/100)
What lifestyle modifications have the most profound effect on dropping BP?
DASH diet (8-14), q10kg wt. loss (5-20), 30 min exercise q5-6x/week (4-9), Na
Best anti-HTN med for AAs? What if they have DM?
AAs = HCTZ. AA + DM = ACE-I is 1st line in all patients with DM due to its renal protective effect
Lifestyle modification necessary for HCTZ to work?
Na restriction, otherwise hypokalemia will be exacerbated
Best anti-HTN med for old men with BPH?
Alpha-blockers
Meds usually tried in patients with HTN refractory to 1st and 2nd line therapy?
Vasodilators (hydralazine and minoxidil) in combination w/beta-blockers and diuretics
Anti-HTN medications contraindicated in pregnancy?
ACE-I, ARBs, CCBs and thiazides. Beta-blockers and hydralazine are safe.
Which anti-HTN is the best 1st line medication?
Unless there is a compelling reason HCTZ, dihydropyridine (CCB), ACE-I and ARBs are all commonly used as initial monotherapy.
ACCOMPLISH trial findings regarding effectiveness of combination therapy
Benazepril + amlodipine was more effective than and ACE-I or CCB alone.
A patient presents with HTN non-responsive to lifestyle modifications and 6 weeks of HCTZ. What is your next step?
Change to a different type of monotherapy before adding on a second medication.
Who gets screening lipid testing?
All adults > 20 yrs q5 years
What are the causes of primary dyslipidemia syndromes? How are they treated?
I) Exogenous HLD = chylomicrons, tx’d w/diet modification. IIa) Familial hypercholesterolemia = LDL, tx’d w/statins, niacin, cholestyramine. IIb) Combined hyperlipoproteinemia = LDL + VLDL, tx’d w/statins, niacin, gemfibrozil. III) Familial dysbetalipoproteinemia = IDL, tx’d w/gemfibrozil, niacin. IV) Endogenous HLD = VLDL, tx’d w/niacin, gemfibrozil, statins. V) Familial hypertriglyceridemia = VLDL + chylomicrons tx’d w/niacin, gemfibrozil
Causes of secondary dyslipidemia?
Endocrine (hypothyroidism, DM, Cushing’s), Renal (nephrotic syndrome), ESLD, Meds (propranolol, HCTZ, estrogen, prednisone) and Pregnancy.
Foods that will elevate LDL
Saturated fatty acids and cholesterol
Foods that will elevate triglycerides (VLDL)?
High calorie diets and alcohol
At what age do cholesterol levels stop increasing?
65
When do both genders have equal risk for HLD?
After menopause
How is LDL measured?
Total cholesterol - HDL - TG/5
LDL levels associated with significant increase in CAD risk
160
Total cholesterol levels associated with significant increase in CAD risk?
160-200, > 240 is really bad
Why is HDL so good?
Every 10mg/dL increase = 50% decrease CAD risk. HDL 60 subtracts 1 point from risk.
Risk associated with total cholesterol to HDL ratio
A patient with DM presents with an LDL of 120, what is your next move?
Old guidelines say all DM patients with LDL > 100 should be on a statin. They should be on a statin if LDL > 70 if they have DM + CAD.
Labs to get routinely if you put your patient on a statin or fibrate?
LFTs, these can cause transaminase elevations. Statin should be discontinued in the setting of elevated transaminases. Note that patients on statins can also get benign CK elevations
Risk of hypertriglyceridemia
Associated w/CAD and pancreatitis
Labs to order when diagnosing someone who came back with a non-fasting elevation in their total cholesterol and drop in HDL?
Full fasting lipid panel (TChol, HDL, TGs, calculated LDL), TSH (hypothyroidism), LFTs (ESLD), BUN/Cr/UA (nephrotic) and HbA1c (DM).
Statins listed most to least potent
Simvastatin/Atorvastatin > Lavastatin/Pravastatin > Fluvastatin
What are the LDL goals in patients with CHD or CHD risk equivalents (PVD, AAA, DM, CAD), no CHD w/>2 risk factors, no CHD w/2 risk factors and no CHD w/
*
What are the CHD risk equivalents that make a patient have a target LDL
DM, PVD, CAD, AAA
What is the most effective lifestyle change you can ask patients to make in order to lower their LDL?
Reduce saturated fat intake, this lowers LDL more than decreased cholesterol intake does. Diet should be
How does exercise help patients with lipidemia?
It increases HDL
How does prescribing a statin to a patient affect their relative cardiovascular risk?
Drops it by 20-30% regardless of baseline LDL
Why are statins so effective?
They reduce LDL AND act as an antioxidant in the endothelial lining of coronary arteries
What levels on the lipid panel are affected by statins? Niacin? Cholestyramine? Gemfibrozil?
Statin: LDL (most potent drug). Niacin: TG, LDL and HDL (most potent drug for TG & HDL). Cholestyramine: LDL, TG. Gemfibrozil: VLDL, TG, HDL.
Medications that can be considered for elevated TGs?
Fibrates, nicotinic acid and fish oil. Statins should be given because they are cardioprotective.
Lipid lowering agent contraindicated in diabetics
Niacin, it may worsen glycemic control
Lipid lowering agent with possible side effects of gynecomastia, gallstones, weight gain and myopathy.
Gemfibrozil
What are the defining characteristics of a tension headache?
Worsens throughout the day, precipitated by anxiety/depression/stress, “band-like” pain around entire head, radiates to neck/upper back w/muscle tightness.
Treatment of tension headaches
Stress reduction, anxiety/depression eval. NSAIDs, Tylenol, ASA are 1st line. Migraine medications can be 2nd line.
What are the defining characteristics of a cluster headache?
More common in men, episodic HA may last 2-3 mo. and remit for years, chronic HA may last 1-2 years. Deep, searing, stabbing unilateral pain behind the eye. Pts may become suicidal. Lacrimation, flushing, nasal discharge. Typically occur a few hours after going to bed and last 30-90 min, awakes from sleep. Worse w/alcohol.
Treatment of cluster headaches
Acute: sumatriptan + O2. Prophy: verapamil is 1st line and works very well. May also use ergotamine, methysergide, Li and prednisone.
What are the defining characteristics of a migraine w/aura?
Bilateral homonymous scotoma, scintillating scotoma, flashing lights, hemiparesis and/or dysphagia
What are the defining characteristics of a menstrual migrain
2 days b/f menses or on the last day of menses due to estrogen withdrawal.
Definition of status migrainosus
> 72 hours w/o spontaneous resolution
What are the defining characteristics of the migraine without aura (common migraine)?
F > M. +FHx. Triggers (stress, anxiety, poor sleep, chocolate, cheese, alcohol, tobacco, OCPs, weather change). Prodrome: CNS excitation or inhibition. Progresses to severe, unilateral, throbbing HA that lasts for 4-72 hours. Worse w/cough, activity or bending over. Associated N/V, photophobia, phonophobia, sensitivity to smell.
Postulated pathogenesis behind migraines
5-HT depletion
A patient presents with a severe, unilateral throbbing headache for the past 10 hours. It is non-responsive to DHE or sumatriptan and he claims to get these headaches often. What is the most likely cause?
Rebound analgesic HA occur every 1-2 days (unlike migraines which occur 1-2x/month) and do not respond to drugs. If he did not have a long hx of these you would consider a more serious etiology
Treatment of an acute migraine attack?
1st line: NSAIDs, Tylenol. 2nd line: dihydroergotamine (DHE, a 5-HT1 agonist) or sumatriptan (more selective 5-HT1 agonist).
When is dihydroergotamine contraindicated?
Pregnancy, CAD, TIAs, PVD and sepsis
When is sumatriptan contraindicated?
Use > 1-2x/week, pregnancy, CAD, uncontrolled HTN, basilar aa migraine, hemiplegic migraine and use of MAOI, SSRI or Li.
Migraine prophylaxis
Used in patients with weekly HA interfering with activities that do not resolve by avoiding triggers. 1st line: amitriptyline, propranolol (most effective). 2nd line: verapamil, valproic acid and methysergide.
Treatment of menstrual migraines
NSAIDs are 1st line. Estrogen supplementation can be added.
What defines a chronic cough and when should further work up begin? What are the most common causes of chronic cough in adults?
> 3 weeks. Failure to resolve in a month should result in further work up. Common causes are smoking, PND, GERD, asthma.
When is ordering a CXR appropriate in a patient with cough?
Chronic cough, suspected pulmonary etiology, hemoptysis or long-term smokers w/suspect COPD or lung cancer
When is bronchoscopy appropriate in a patient with cough?
No dx after CXR, CBC or PFTs. Suspected tumor, web/ring or foreign body.
Tx for post-nasal drip
1st gen. antihistamine/decongestant. +/- abx if sinusitis is present. +/- non-sedating long-acting antihistamine like loratadine if allergic rhinitis
When to use non-specific antitussives? What are they?
Unknown cause, ineffective specific tx or cough serves no purpose. Codeine, dextromethorphan and Benzonatate capsules
When to get labs and rads in a patient with acute bronchitis?
CXR and CBC is pneumonia is suspected +/- ABGs. If you only suspect acute bronchitis, labs/rads are not indicated.
Tx of acute bronchitis
Supportive
Viruses that are common perpetrators in the common cold (acute rhinosinusitis)?
1) Rhinovirus (50%, 100 different serotypes. Others include parainfluenza, adenovirus, coronavirus, coxsackie and RSV
Features concerning for secondary bacterial sinusitis or pneumonia in patients with acute rhinosinusitis?
Fever in an adult
Tx for acute rhinosinusitis
Hydration to loosen up secretions, analgesics (ASA, ibuprofen, acetaminophen), anti-tussive, decongestant nasal spray for
Common causes of acute sinusitis?
Follows URI/common cold or causes it to persist beyond 8-10 days, polyps, deviated septum or foreign body
Common bacteria that cause bacterial sinusitis
S. pneumo, non-typeable H. flu, anaerobes
Sinuses most commonly affected in bacterial sinusitis
Maxillary
Features of chronic sinusitis
At least 2-3 months of nasal congestion, PND usually w/o HA, pain or fevers and hx of multiple sinus infections.
A patient presents with 6 mo of nasal congestion and PND w/a PMHx significant for multiple sinus infxns. How should you treat this patient?
Broad-spectrum penicillinase resistant abx to cover S. aureus and possible GNRs. Refer to ENT.
Complication of ethmoid sinusitis
Orbital cellulitis
Complications possible in all types of sinusitis
Mucocele, polyps, osteomyelitis, cavernous sinus thrombosis, epidural abscess, subdural empyema, meningitis and brain abscesses
A patient presents with a cold for 8-10 days with painful sinuses and nasal congestion. Physical exam reveals purulent drainage from the left turbinates and impaired maxillary sinus transillumination. How do you treat this patient?
This patient has acute sinusitis. Tx with saline nasal spray to help with drainage, pseudoephedrine or oxymetazoline for decongestion for
Common bugs involved in laryngitis?
Mostly viral, M. cat and H. flu can also be involved
Tx of laryngitis
Self-limiting, rest voice to avoid formation of vocal cord nodules
Most common cause of pharyngitis?
Viruses (adeno, para, rhino, EBV and HSV). GABHS is only a concern for tx due to possibility of rheumatic fever, not the pharyngitis.
Other bacterial causes of pharyngitis
Chlamydia, mycoplasma, gonococci, c. diphtheriae and candida (if immunosuppressed)
DDx in a patient w/sore throat
Viral infxn, tonsillitis, strep throat and mono
50:50 pharyngitis rule
Only 50% of patients w/exudates have strep and only 50% of patients w/strep have exudates
Work up in a patient w/strep throat
CENTOR criteria, +/- rapid strep swab. If rapid strep swab is positive treat, if negative culture. +/- mono spot blood test
Tx of strep throat
10 days PCN or erythromycin
Tx of mono
Rest, tylenol/ibuprofen avoid contact sports
Tx of viral pharyngitis
Symptomatic (acetaminophen, ibuprofen, salt water gargle, humidifier, throat lozenges)
A patient presents with heartburn, bloating and epigastric discomfort. What are the most common causes of her condition?
She has dyspepsia. 90% of patients who present with dyspepsia have PUD, GERD, gastritis or non ulcer dyspepsia. Other less common causes include hepatobiliary disease, malignancy, pancreatic disease, esophageal spasm, hiatal hernia, lactose intolerance, malabsorption, DM w/gastroparesis and IBS.
Dx of nonulcer dyspepsia
Dyspepsia for at least 4 weeks and no other dx after endoscopy
Indications for endoscopy in patients presenting w/dyspepsia
Red flags (wt loss, anemia, dysphagia, hematemesis), new onset dyspepsia if > 45 years, recurrent vomiting, no response to empiric therapy
Tx of dyspepsia in a pt w/negative H. pylori testing
Avoid alcohol, caffeine, tobacco, avoid eating before sleep and raise the head of the bed. Add H2 blocker, PPI or sucralfate. Endoscopy if medical therapy fails.
Types of testing used for H. pylori
Gold standard = endoscopy w/biopsy. Convenience = urease breath test (95% sen and spec), documents active infection. Serology = lower specificity b/c ab presence does not = active infection, abs can remain elevated for months to years after eradication, 90% sensitive.
Things to look out for in H. pylori testing that may cause false negative results
PPIs, bismuth, many abx and upper GI bleed
Tx of dyspepsia in a pt w/positive urea breath test
Triple tx: PPI, amox, clarithromycin 10-14 days. Quad tx for retreatment: PPI, bismuth and 2 abx.
A 40 year old woman presents with retrosternal chest pain associated with meals that is worse when lying down. She has associated regurgitation occasionally and salivary hyper secretion (water brash). What is the DDx for her condition?
She has GERD which can be secondary to decreased esophageal motility, gastric outlet obstruction, hiatal hernia, decreased LES tone (idiopathic or alcohol, tobacco, chocolate, fatty foods and coffee).
How is GERD diagnosed?
Gold standard = 24-hour pH monitoring is most sensitive and specific. Endoscopy w/biopsy if heartburn is refractory to tx or +red flags. Upper GI barium contrast study if suspicious for strictures/ulcerations. Esophageal manometry if suspected motility disorder
Barrett’s esophagus
10% of patients w/chronic reflux (> 5 years) develop metaplasia of the distal esophagus from squamous epithelium to columnar epithelium that carries an increased risk for adenocarcinoma
Screening and tx for Barrett’s
Endoscopy w/biopsy if GERD sx > 5 years in duration. If +Barrett’s metaplasia but -dysplasia then screening endoscopy q3 years. Tx = chronic PPI
Cytologic findings that can diagnose recurrent pneumonia due to aspiration in GERD patients
Lipid-laden macrophages
Key physical exam findings in patients w/GERD
Pitting of dental enamel, night time cough, metallic taste in mouth
Tx of GERD
Phase I: lifestyle changes w/antacids after meals and before bed. Phase II: add an H2 blocker. Phase III: switch H2 blocker to PPI if no resolution or pt has erosive esophagitis. Phase IV: add metoclopramide (DA antagonist) or bethanechol (cholinergic agonist) for motility. Phase V: Combo therapy (H2 + promotility, PPI + promotility, +/- increased dose of H2 or PPI). Phase VI: Nissen fundoplication if intractable disease, respiratory problems or esophageal injury.
Tx for a patient w/chronic GERD and new onset dysphagia
They likely have peptic strictures and will need dilation
Definition of acute vs chronic diarrhea
4 weeks
Most common bugs involved in acute diarrhea
Rotovirus and norovirus.
Most common bugs involved in severe acute diarrhea
Bacteria (typically diarrhea is accompanied by fever and blood): Shigella, enterohemorrhagic E. coli, enterotoxic E. coli (no fever/blood), Salmonella, Campylobacter, C. perfingens (no fever/blood), staph aureus food poisoning (no fever/blood), C. difficile. Protozoa: Giardia, Entamoeba, Cryptosporidium.
Common bugs involved in acute diarrhea in the immunocompromised
MAI, Cryptosporidium, Cyclospora, CMV
Aside from infection what are common causes of acute diarrhea?
Antibiotics: esp. clinda, amp and cephalosporins. Meds: laxatives, prokinetics (cisapride), antacids, digitalis, cochicine, alcohol, Mg, chemo. Malabsorption. Ischemic bowl. Tumors.
Common causes of chronic diarrhea
1) IBS. Others include IBD, meds, infection, colon cancer, diverticulitis, malabsorption, post surgical (vagotomy, gastrectomy), endocrine (hyperthyroid, Addison’s, DM, gastrinoma, VIPoma), fecal impaction and laxative abuse.
Indications for lab work up in patients with diarrhea? What labs?
Usually none is required unless diarrhea is chronic, pt is severely ill, there is blood in the stool, peritonitis, immunodeficient or volume depleted. Labs: CBC, stool sample for fecal leukocytes, stool culture for C. difficile/shigella/salmonella/campylobacter if +leukocytes, O&P x 3 if suspect parasite +/- giardia ELISA, stool for C. difficile toxin assay.
Why do bacterial stool cultures kind of suck?
Fecal leukocytes are only positive if the infection is due to campylobacter, salmonella, shigella, EIEC or C. difficile. There are no + fecal leukocytes w/staph, c. perfringens or viruses and consequently due to the algorithm no culture will be done for these patients. Additionally, if you do a culture, there is a low sensitivity.
Most common electrolyte abnormality in patients with diarrhea
Metabolic acidosis + hypokalemia
4 reasons to admit a patient w/acute diarrhea
Unable to tolerate PO, bloody diarrhea, toxic appearing, volume deplete
Treating acute diarrhea
Rehydrate + correct electrolytes, NPO trial, 5-day course of cipro for patients w/moderate to severe sx (high fever, bloody stools, +cx, traveler’s diarrhea), give PO metronidazole or vanc if C. difficile. Only giver loperamide if diarrhea is mild to moderate w/no fever or blood.
A patient presents to the clinic with diarrhea for the past 48 hours, myalgia, malaise, nausea and vomiting. He has family members w/similar sx. Physical exam reveals a low-grade fever. Labs show no fecal leukocytes. What is the most likely diagnosis?
Acute viral gastroenteritis (norwalk or rotavirus)
A patient presents to the clinic with a 48 hours hx of diarrhea, abdominal pain, nausea and vomiting. He admits to eating raw eggs. On physical exam he has a fever. Labs are +for fecal leukocytes. What is the most likely dx and how do you treat?
Salmonella. No tx necessary unless suspect typhoid fever, then tx w/cipro (also tx if immunocompromised).
A patient presents to the clinic with 48 hour hx of diarrhea, tenesmus and abdominal pain. On physical exam he has a fever. Labs are + for fecal leukocytes. How will you likely treat this patient?
Bactrim, he likely has shigella which commonly presents w/tenesmus
A patient presents with a 6 hour hx of abdominal pain, diarrhea, nausea and vomiting. He has no fever and stool leukocytes are negative. He admits to eating potato salad 6 hours ago. How do you treat this guy?
He likely has staph food poisoning, supportive tx is appropriate.
A patient presnets with 48 hour hx of HA that just recently was followed by diarrhea and abdominal pain. He admits to blood in his stool. He has a fever and + stool leukocytes. How do you treat him?
He likely has been infected by campylobacter and needs erythromycin.
A patient presents with a 12 hour hx of crampy abdominal pain and diarrhea. He ate chinese food prior to onset of sx. He does not have a fever and negative stool leukocytes. What is causing his sx?
C. perfringens
A patient presents with watery diarrhea, nausea and abdominal pain for 48 hours. He just returned from Mexico. He does not have a fever and stool leukocytes are negative. What is causing his sx?
Enterotoxic E. coli
A patient presents with 24 hours of bloody diarrhea and is very toxic appearing. He has a fever and admits to eating undercooked meat at a barbecue. Stool leukocytes are positive. What are major complications associated with his infection?
He likely has been infected by E. coli O157:H7 which is typically self-limited, but can be complicated by hemolytic uremic syndrome and thrombotic thrombocytopenic purpura.
A patient presents with 5 days of watery, foul-smelling diarrhea and bloating. He recently went hiking and does not have a fever and has negative stool leukocytes. How do you treat him?
He likely has giardiasis. Tx w/metronidazole.
A patient presents with rice water stools, abdominal pain and vomiting. He has a low-grade fever and negative stool leukocytes. What is likely causing his condition?
Vibrio cholera