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internal medicine nbme shelf > im > Flashcards

im Flashcards

1
Q

emergent tx for hyperkalemia

A

hyperkalemia is treated emergently when ECG changes (peaked t waves, widened QRS, bradycardia, disappearance of p waves, sinus node dysfunction and av node block) or when K+ is really high (like >6.5) or rises really fast. Calcium is used to stabilize cardiac membrane. Since it’s faster to shift K+ intracellular than get it out of the body, insulin is given. Glucose is also given to prevent hypoglycemia.

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2
Q

acute epididymitis usually due to bladder obstruction and the organism ______ in men >35 and due to ________ in men <35

A

men >35: e coli men < 35 N gonorrhea, Chlamydia

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3
Q

dermatomyositis antibodies

A

anti RNP, anti JO 1, anti Mi2 bonus: highly elevated creatinine kinase

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4
Q

in patients wither dermatomyositis, you need to screen for…

A

internal malignancy! they are at much higher risk for cancer also interstitial lung disease, myocarditis, dysphagia

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5
Q

seen with heliotrope rash, proximal muscle weakness, rash on shoulders

A

dermatomyositis

anti RNP, anti Jo 1, anti Mi2

give high dose glucocorticoid steroid plus glucocorticoid steroid sparing agent and screen for malignancy

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6
Q

how do you tell the difference between IgA nephropathy and acute post infectious glomerulonephritis?

A

both are nephritic syndrome (blood in urine, htn). Ig A nephropathy will affect Adults (20s-30s usually men) while postinfectious GN usually affects kids ages 6-10. IgA nephropathy shows up 5ish days after an infection while postinfectious GN takes weeks after an infection and it’s usally strep throat or impetigo so check their antistretolysin O titers. Also in IgA nephropathy complement levels are normal while in postinfectious GN complement levels are low. both tend to have benign course but IgA nephropathy can cause rapidly progressive glomerulonephritis and postinfectious GN can possibly lead to CKD in adulthood

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7
Q

triad of paroxysmal nocturnal hemoglobinuria

A
  1. hemolytic anemia
  2. pancytopenia
  3. thrombosis (especially in weird places like in abdomen, hepatic, cerebral)

usually in middle age b/c acquired mutation, lack CD55, CD 59 on RBCs, tx: prednisone and eculizumab

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8
Q

describe cardinal symptoms of ACA, MCA, posterior, opthalmic, lacunar stroke syndromes

A
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9
Q

high fever, severe polyartheritis, lymphopenia & thrombopenia, macular rash 3-7 days after travel to tropical/subtropical regions of central/south america, asia, africa

A

chikungunya fever

transmitted by mosquito (Aedes)

supportive care

often causes chronic arthritis, may have to give methotrexate

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10
Q

opening snap with mid diastolic rumble heard best at the apex

A

mitral stenosis,

most commonly due to rheumatic fever (usually in immigrants)

-can cause right sided, heart failure, dyspnea, left atrium dilation –> bronchus elevation and afib

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11
Q

Think of new onset afib with RVR as a different disease than chronic afib. What do you do for someone with new onset afib with RVR?

A
  1. Are the symptomatic? Presumably yes or you wouldnt get called
  2. Are they unstable? Like will they die in seconds? If yes, you shock – synchronous cardioconversion. They will need anticoag for a month afterwards
  3. Much more likely scenario: symptomatic and stable: You need to RATE CONTROL. Goal: below 110. Here’s the all important question: are they in heart failure exacerbation or not?

Acute decomp HF: Give Digoxin or Amiodirone

No HF: CCB like diltiazam or beta blocker like metopropolol

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12
Q

Think of new onset afib with RVR as a different disease than chronic afib. What do you do for someone with chronic afib

A

per AFFIRM trial, you can either do rate or rhythm control. Really the only time you’ll do rhythm control is for somebody who has “no good reason”to be in afib and won’t hop right back into if you convert them out and you’ll for sure anticoag those peeps.

For rate control: diltiazem or metroprolol.

Anticoag? CHA2DS2VAS score >2

for score of 1, maybe, maybe aspirin, maybe nothing

Anticoag:

Warfarin: No bridge needed for afib. Reversible. Inconvenient. Have to worry about diet. INR 2-3.

NOACs: Dabigatran, Apixiban, Rivaroxaban: easier, no reversal, insurance?

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13
Q
A
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14
Q

most common site of ectopic electrical foci causing afib

A

pulmonary veins

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15
Q

most common anatomic origin of atrial flutter

A

tricuspid annulus

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16
Q

status of pt with + Anti-HepB surface antibody and +Anti HepB core antibody and -HebBeAg

A

AntiHepB core antibody is present in acute or chronic infection but NOT after immunization; Anti-HepB surface antibody is present after immunization or succesfully clearing an infection so this person succesfully cleared an infection.

HepB e Ag indicates active infection and viral replication, infectivity

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17
Q

You have a patient with atypical community acquired pneumonia, GI symptoms and confusion – what tests would be really helpful besides the usual labs?

A

likely Legionnaire’s disease, especially if history of travel

Sputum culture Gram stain: lots of neutrophils, no organisms

Urinary legionella antigen

also low Na+ on BMP

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18
Q

acute symmetric arthritis in a school teacher/day care worker, maybe fever, fatigue, diarrhea

A

Parvovirus B19

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19
Q

describe areas of referred abdominal pain

A
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20
Q

test for suspected urolithiasis

A

abdominal US or noncontrast spiral CT

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21
Q

why is colonoscopy usually not performed in pts with acute abdominal pain

A

risk of perforation

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22
Q

what are 3 most common causes of esophogitis in patients with HIV?

A
  • Herpes simplex virus
  • candida
  • CMV

How do you tell the difference? In Candida albicans, they will usually have oral thrush as well so that one is easy. For VIRAL esophogitis, the primary complaint is PAIN with swallowing but they can still swallow.

HSV: usually ulcers around mouth, round volcano-like ulcers in esophagus

CMV: linear ulcerations in esophagus

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23
Q

symptoms of hemorrhagic stroke in cerebellum

A

ipsilateral ataxia

nystagmus

occiputal headache, maybe neck stiffness

NO hemiparesis

facial weakness

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24
Q

symptoms of hemorrhagic stroke in Thalamus

A

contralateral hemiparesis and hemisensory loss

eyes deviate Toward hemiparesis

upgaze palsy

nonreactive miotic pupils

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25
Q

Pons coma symptoms

A

deep coma, total paralysis happens in minutes, pinpoint reactive pupils

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26
Q

symptoms of occipital lobe stroke

A

contralateral homonymous hemianopsia

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27
Q

euthyroid sick syndrome

A

happens in acutely ill patients, problems converting T4–> T3 in periphery

usually normal TSH and T4 but low T3 but everything can be low in extreme cases

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28
Q

pulmonary capillary wedge pressure is a measure of

A

left ventricle end diastolic pressure

elevated in left ventricle dysfunction

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29
Q

Name 3 complications of cirrhosis with portal hypertension

A

ascites

spontaneous bacterial peritonitis

variceal bleeding

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30
Q

cor pulmonale = impaired right heart function due to chronic lung disease

Name cor pulmonale signs and diagnostic tests

A

Elevated JVP

hepatomegaly, pulsatile liver

tricuspid regurgitation

right ventricular 3rd heart sound

edema in lower limbs

ascites

pleural effusions

Increased right heart pressures on ECHO, raised pulmonary artery systolic pressure on heart catheterization

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31
Q

back pain that gets better with sitting/walking uphill and worse with standing/walking downhill

A

spinal stenosis (better with flexion and worse with extenion)

MRI

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32
Q

asymmetric arthritis (even with warm swollen joints with leukocytes ), mouth ulcers, urethritis, conjunctivitis, low back pain

A

reactive arthritis

treat with NSAIDS

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33
Q

name 6 complications of ulcerative colitis

A
  1. spondyloartheritis
  2. colorectal cancer
  3. toxic megacolon
  4. erythema nodosum, pyoderma gangranosum
  5. uveitis
  6. primary sclerosing cholangitis
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34
Q

which type of IBD has skip lesions

A

chrons disease

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35
Q

age of presentation of ibd

A

bimodal

15-40 and 50-80

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36
Q

pt with large mediastinal mass

eosinophila

chest pain when drinking EtOH

elevated lactate dehydrogenase

A

Hodgkin lymphoma

elevated LDH associated with high tumor burden

remember to look for Reed Sternberg cells

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37
Q

what can happen when someone with myasthenia gravis has an infection?

A

myasthenic crisis

infection, surgery, preg/childbirth, tapering immunosuppressive drugs, certain meds lik beta blockers or aminoglycosides leads to extra muscle weakness. Watch out, they might be in serious respiratory distress but you don’t notice because they arent strong enough to struggle for air. Features might include dysphagia and choking sensation because they can’t clear secretions. Respiratory acidosis. They might be on death’s door before you realize it. Intubate. Plasmapharesis or IVIG. Corticosteroids.

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38
Q

transplanted kidney with recent increase in creatinine, proteinuria. On biopsy, lymphocyte infiltration of the intima, inflammatory tubular disruption, intimal arteritis. Transplant less than 6 months ago and pt is asymptomatic. What is it and what do you do?

A

Acute transplant rejection (predominantly T cell mediated)

mostly reversible

give high dose glucocorticoids and increase immunosuppressive doses

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39
Q

pt with kidney transplant. Pt is asymptomatic but has recent increase in creatinine. Biopsy shows intranuclear inclusions and mixed neutrophils and lymphocyte infiltration

A

BK virus reactivation due to immunosuppression

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40
Q

severe headache that came on within a few minutes with photophobia and vomiting and neck stiffness. Noncontrast CT is negative.

A

Get lumbar puncture to rule out subarachnoid hemorrhage.

Signs of SAH on LP: high opening pressure, xanthochromia (yellow-pink color), lots of RBCs

CT is sensitive for bleeds but might not pick up smaller or older bleed

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41
Q

rash

fever

AKI

eosinophilouria + WBC casts

A

interstitial nephritis

usually due to drugs

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42
Q

According to AHA, who gets a statin? (name 4)

A

If you are 40-75 and have diabetes

pts with known ascvd, stroke/tia, pad, other coronary revascularization procedure…

LDL >190

40-75 with ascvd 10 year risk >7.5%

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43
Q

symptoms/signs of the most common side effect of statins

A

myopathy

elevated CK

tender muscles

(you can also get elevated liver enzymes!)

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44
Q

which antilipid drug is best at raising HDL

A

niacin

remember can cause flushing and tachycardia so best to take aspirin first

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45
Q

fenofibrate and gemfibrozil are fibric acid derivatives used to lower triglycerides. What are their side effects?

A

gallstones! raised LFTs! and other gi effects

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46
Q

acute coronary syndrome pathophysiology

A

usually in situ thombosis at the site of ruptured athrosclerotic plaque

can also be due to thromboembolism causing occlusion, vasospasm, vasculitis, aortic root or coronary artery dissection, or cocaine use (cause both vasospasm and thrombobosis)

unstable angina happens when the thrombosis doesnt cause complete occlusion or there is spontaneous lysis; in chronic stable angina there is usually stenosis from an athrosclerotic plaque that’s only a problem when demand is increased due to exercise

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47
Q

in setting of MI, S4 suggests….

S3 suggests….

*persistent* ST elevation suggests….

A

S4 suggests noncompliance of the ventricles due to ischemia

s3 gallop is severe systolic dysfunction

*persistent* ST elevation is left ventricular aneurysm

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48
Q

what’s the difference in pathophysiology of STEMI vs NSTEMI

A

in STEMI we’re talking transmural ischemia whereas in NSTEMI it’s usually subendocardium

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49
Q

ST elevation in leads II, III, aVF suggests a problem where….

A

inferior surface of heart

supplied by right coronary artery

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50
Q

ST elevation in V2 V3 and V4 suggests a problem where?

A

anterior aspect of heart supplied by left anterior descending artery

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51
Q

ST elevation in I, aVL, V5, V6 suggests a problem where?

A

lateral aspect

supplied by lateral circumflex coronary artery

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52
Q

physical exam findings of aortic dissection

A

unequal pulses and BPs in each arm

widened mediastinum

murmur of aortic insufficiency

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53
Q

pericarditis ECG finding

A

diffuse ST elevation (not by vascular distribution like we see in MI)

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54
Q

MI Tx

A
  • anticoagulation: aspirin, heparin
  • beta blockers to lower demand
  • nitrates to increase coronary blood flow

all of the above reduce mortality

patients may also be given morphine for the pain and tachycardia as well as oxygen

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55
Q

If pt with acute STEMI presents within 2-3 hours of symptom onset and receive ___ ideally within 90 minutes, then ____is the recommended reprofusion therapy

A

PCI, percutaneous reprofusion intervention

also appropriate if contraindication for thrombolytics, hypotensive or in cardiogenic shock

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56
Q

what are two most common causes of death in setting of an MI

A

ventricular arrythmia

cardiogenic shock (pump failure)

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57
Q

unilateral headache, ipsilateral Horner syndrome (ptosis and constricted pupil)

A

carotid dissection

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58
Q

headache, lethargy, photophobia, vomiting, CN palsy

A

subarachnoid hemorrhage

saccular aneurysms can compress CNs, for example compression of CNIII can cause one pupil to be dilated (think rupture of posterior communicating artery), compression of CNII can cause vision loss (internal carotid or anterior communicating artery), or compression of CN IV (trochuler) by superior cerebellar artery

or CNVI abducens by inferior cerebellar artery

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59
Q

blowing highpitched holosystolic murmur heard at apex plus S3

A

severe mitral regurgitation

Due to backflow of blood from LV to LA during systole (because mitral valve is jacked), the total amount of blood entering LV during systole each time goes way up. To compensate, the LV undergoes eccentric hypertrophy. The apical impulse will probably be displace to the left on palpation. The S3 happens when all that increased volume rushes into the dilated floppy LV and slams against the wall during systole. S3 is highly suggestive of severe mitral regurg and its absence helps rule out severe mitral regurg. Pts with bad mitral regurge will start to develop dyspnea because the floppy dilated LV has decreased output. They will also get pulmonary hypertension eventually.

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60
Q

wide fixed splitting of S2 occurs with…

A

atrial septal defect

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61
Q

what type of hypersensitivity reaction is this and what causes it?

A

this is erythema multiforme and it is type IV hypersensitivity (delayed Tcell mediated)

Herpes simplex virus, Mycoplasma pneumonia

medications like Phenytoin, beta lactams (e.g penicillins), sulfonamides

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62
Q

a lot of people with cirrhosis wind up with esophogeal varices and 1/3 of ppl with esophogeal varices wind up with hemorrhage. So most ppl with cirrhosis should get diagnostic upper endoscopy to look for varieces. If nonbleeding varices are found, what is 1st line prophylaxis to prevent progression?

A

beta blockers

eg propranolol, nadolol

(endoscopic variceal ligation is alternative if beta blockers contra indicated)

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63
Q

patient with few symptoms over months to years, palpable spleen, huge leukocytosis and low leukocyte alkaline phosphatase

A

low leukocyte alkaline phosphatase should make you think CML, chronic myeloid leukemia. Low leukocyte alkaline phosphatase distinguishes CML from leukomoid rxn and all other leukemia!

most commonly caused by t(9;22) translocation (Philadelphia) –> BCR-ABL fusion protein that is constitutively active protein kinase

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64
Q

if you suspect lymphoma what do you always do?

A

cut it out! excisional biopsy is a must

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65
Q

older patient with increased hematocrit, leukocyte count, and platelet count. +pruritis, dizziness, headaches, blurred vision.

what’s going on? what are potential complications? how do you treat?

A

Polycythemia vera caused by JAK2 mutation

complications: usually goes on for a long time without problem and then you get hypercoagulable –> thrombosis–> stroke

Treatment: repeated phlebotomy until you get hematocrit below 45% + aspirin

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66
Q

if you think your patient has CML, what should you do next?

A

get cytogenetic studies so you can see if they have t(9;22) BCR-ABL which has targeted therapy

imatinib

dasatinib

nilotinib

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67
Q

imatinib

A

targeted against BCR ABL in CML

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68
Q

dasatinib

A

targeted against BCR ABL in CML

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69
Q

nilotinib

A

targeted against BCR ABL in CML

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70
Q

Leukomoid reaction

what causes it?

lab findings?

A

Leukomoid reaction: extreme leukocytosis with increase in all of the cell lines and increase in leukocyte alkaline phophatase (LAP) score. (Decreased in CML)

Often secondary to solid tumor like lung or kidney, infections, drugs like steroids

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71
Q

older patient with lymphocytosis

smudge cells on smear

B cells with CD19, CD20, CD23 on flow cytometry

A

CLL, chronic lymphocytic leukemia

usually just watch!! patients are usually asymptomatic when diagnosed and chemo is just for symptoms not for increased survival. very slow moving malignancy

if you do tx: fludarabine, cyclophosphamide, rituximab

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72
Q

A_L is most common leukemia of childhood

A_L is most common acute leukemia of adulthood

A

ALL kids

AML adults

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73
Q
A

Auer rods

acute myeloid leukemia (myeloperoxidase positive)

t(15;17) common

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74
Q

pathophysiology of myasthenia gravis

A

autoantibodies against acetylcholine receptors at neuromuscular junction

treatment is cholineasterase inhibitor: pyridostigmine

2nd line: glucocorticoids

ptosis improved with ice pack over eyes bc it slows down breakdown of acetylcholine

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75
Q

first line tx for myasthenia gravis

A

pyridostigmine (cholinesterase inhibitor)

2nd line is glucocorticoid

IVIG/plasmapharesis in crisis

thymectomy in some cases

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76
Q

Name symptoms and treatment of hypercalcemia

A

Bones, abdominal groans, moans, neuropsychiatric overtones: Bone pain, GI distress, weakness, confusion, lethargy, stupor

For severe, **symptomatic** hypercalcemia: IV Saline hydration!!! you want to dilute that calcium. also CALCITONIN (tone down the calcium). (only if they are crazy volume overloaded will you give furosemide)

Long term: Bisphosphonates.

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77
Q

symtpoms of CO poisoning

lab signs

treatment

A

confusion, wheezes, dyspnea, nausea, headache

seizure, coma, cherry red lips

anion gap metabolic acidosis

**pulse oximeter usually normal bc can’t distinguish oxyhemoglobin from carboxyhemoglobin

can cause irreversible hypoxic brain damage

100% oxygen through nonrebreather face mask, hyperbaric O2 in extreme cases

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78
Q

How can you prevent renal calcium stones?

A

low sodium diet

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79
Q

pesticide (organophosphate) poisoning mechanism, symptoms, antidote

A

cholinergic stimulation (both muscarinic and nicotinic)

SLUDGE: Salivation (also secretion in lungs), Lacrimation, Urination, Diaphoresis/Diarrhea, GI distress/Gasping for air, Emesis

Atropine followed by Pralidoxime

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80
Q

what should you suspect if someone has blood on urine dipstick but no RBCs on urine microscopy

and elevated [K+] and [PO4]?

A

rhabdomyolysis

think crush injury, intense mm activity including seizures, drug toxicity including statins

lysed mm fibers release potassium and phosphorous

causes AKI, tubular necrosis

increased AST>ALT

dx made by hugely elevated CK

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81
Q

stroke that causes pure sensory loss and then weeks later may cause allodynia => severe burning pain at light touch to contralateral limbs

A

thalamus

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82
Q

symptoms of lateral medulla stroke

A

Wallenberg syndrome

temperature regulation probs

horner syndrome (ptosis, miosis, anhidrosis)

*crossed sensory deficit (ipsilateral face, contralateral body)

ataxia

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83
Q

criteria for starting long term O2 for ppl with COPD

A

-sat 88% on room air at rest

or

-sat 89% at rest with cor pulmonale or hematocrit >55%

(remember secondary polycythemia can result from chronic hypoxemia)

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84
Q

Name 2 tests to make MS diagnosis

A

T2 MRI - look for lesions disseminated in time and space

IgG oligoclonal bands on CSF analysis

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85
Q

describe 4 common types of MS symptoms/lesions

A
  • “optic neuritis” mononuclear vision loss, afferent pupillary defect
  • transverse myelitis – loss of function below of certain spinal level. first flacid paralysis (spinal shock) followed by spastic paralysis c hyperreflexia. often incontinence
  • internuclear opthalmoplegia - demylelination of medial longitudinal fasiculus; the eye on the same side as the lesion cant adduct towards the nose and the eye on the contralateral side abducts with nystagmus
  • cerebellar dysfunction: ataxia, intention tremor, nystagmus
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86
Q

what do you give elderly patients with dementia for delierium in the hospital?

A

low dose haldol

can also do quetiapine, risperadone

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87
Q

what to do for esophagitis symptoms in a pt with HIV and oral thrush?

A

empiric treatment for Candida esophagitis: oral fluconazole. If it doesn’t get better you can do endoscopy, culture/cytology and look for viral etiology. Remember that linear ulcers point to CMV and volcano like ulcers point to HSV. Treat CMV with ganciclovir and HSV with acyclovir

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88
Q

healthy kid with very low platelet count

A

isolated thrombocytopenia, usually due to autoimmune thrombocytopenia

a diagnosis of exclusion

usually healthy kids 2-5 or teens. Everything is normal but platelet count.

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89
Q

what is considered a narrow QRS (in ms)? what is considered a wide QRS?

A

narrow qrs is <.12 ms (three little boxes)

wide qrs is greater than 0.12 ms (three little boxes)

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90
Q

what rhythm is this? what do you do for it?

A

sinus bradycardia

if unstable, pace

if stable and symptomatic, adenosine

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91
Q

what is length of normal PR interval on ECG?

A

0.12-0.2 ms (3 to 5 little boxes)

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92
Q

what rhythm is this? what do you do for it?

A

1st AV block – the PR interval is prolonged and no beats are dropped. if the patient is unstable, you pace them (unstable signs: LOC, AMS, hypoperfusion, shock, pulmonary edema)

if stable, you can use adenosine

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93
Q

what rhythm is this? what do you do about it?

A

This is 2nd degree AV block type 1 (Mobitz 1)

the PR interval gets longer and longer until a beat is dropped.

If unstable, pace; otherwise give adenosine or atropine (anticholinergic)

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94
Q

what are causes of AV block?

A

Ischemia! STEMIs, acute coronary syndromes

infectious diseases: Chagas, Lyme, endocarditis, acute rheumatic fever, diphteria, toxoplasmosis

inflammatory/infiltrative diseases: myocarditis, sarcoidosis, rhemautic diseases like SLE, sclerosis, rheumatic artheritis, reactive artheritis,

cardiac procedures

congential

metabolic/endocrine probs like thyroid

certain drugs like beta blockers, digoxin, calcium channel blockers…

and more!

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95
Q

what rhythm is this? what do you do?

A

This is AV block type II (Mobitz II)

Prolonged PR with random dropped beats

tx: try to identify and remove underlying cause, e.g. a medication

for acute management: usually atropine and pacing

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96
Q

what rhythm is this? what do you do?

A

This is 3rd degree AV block; there is no AV conduction

definitely permenant pacing

medical therapies include atropine, beta adrenergic agonists like dopamine, dobutamine, isoproterenol, epinephrine ; also IV aminophylline

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97
Q

what rhythm is this? what do you do?

A

idioventricular rhythm – ventricles running the show but it’s not vtach. So notice slow rate but complete absence of p waves

i think the answer is pacing? same meds as other serious av blocks?

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98
Q

what rhythm is this? what do you do?

A

supraventricular tachycardia

notice fast rhythm, ABSENCE OF P WAVES, narrow QRS

Pathophys: usually some reentry pathway around AV + exacerbating factor

If unstable: SHOCK -synchronized cardioversion

If stable: try Vagal maneuver, IV adenosine

diltiazem, verapamil, propranolol, metropolol

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99
Q

After defibrillation, an ecg of sinus rhythm shows prolonged QT interval (this tidbit important!)

what rhythm is this? what do you do?

A

torsades de pointes

Note that this polymorphic vtach is not proven torsades if you don’t know there is underlying QT prolongation

I gave away treatment: If unstable: shock. If “stable” – give IV magnesium but stay close and be ready to shock.

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100
Q

what is considered prolonged QT?

A

>450-470 ms

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101
Q

Name antidepressants that can prolong qt

A

citalopram, escitalopram, TCAs

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102
Q

what rhythm is this? what do you do?

A

ventricular tachycardia

causes: structural heart probs including old infarct scars; congenital stuff like congenital long QT or hypertrophic cardiomyopathy; reversible causes like electrolyte imbalance, drugs, acute ischemia, hypoxia

Unstable: SHOCK

Stable: IV procainamid, IV amiodarone, or IV sotalol to try to stop Vtach

urgent catheter ablation

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103
Q

MI patient with cold extremities, elevated JVP, crackles, hypotension (systolic <80), high left and right filling pressures (measured indirectly with pulmonary capillary wedge pressure >18mmHg)

A

Cardiogenic shock

oxygen, vasopressors like dobutamine and dopamine, might also need reduce afterload through intra aortic balloon counterpulsation and iv nitroglyverin or nitroprusside

might have to do urgent revascularzation with PCI

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104
Q

MI patient with markedly elevated JVP, hypotension, but clear lungs

A

right ventricular infarction, tends to be a complication of inferior STEMIs

The first step to spotting RV infarction is to suspect it… in all patients with inferior STEMI!

In patients presenting with inferior STEMI, right ventricular infarction is suggested by the presence of:

ST elevation in V1 – the only standard ECG lead that looks directly at the right ventricle.

ST elevation in lead III > lead II – because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle.

RV infarct is very preload sensitive DO NOT GIVE NITRATES

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105
Q

Name 3 MI complications that would cause systolic murmurs

A
  1. papillary muscle dysfunction –> mitral regurg
  2. papillary muscle rupture–> flail mitral leaflit and acute mitral regurg–> cardiogenic shock and heart failure
  3. new holosystolic murmur due to ventricular septal rupture

these usually happen in the first week

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106
Q

what should you suspect if ECG still shows ST elevation several weeks after an MI?

A

ventricular anuerysm

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107
Q

Dressler syndrome is a complication of MI that occurs several weeks later. What are symptoms?

A

Pleuritis

Pericarditis

Fever

(immune mediated)

tx with nsaids, sometimes prednisone

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108
Q

drugs for someone having a heart attack

A

MONA BASH C

Morphine

O2

Nitrates (unless you think its RV)

Asprin

Beta blocker

ACE-i

Statin

Heparin

Clopidegrel

underlined = they should def go home on; they might also go home on nitrates if chest pain; they will go home on clopidagrel for 1 year if they have drug eluding stent and for 1 month if they have bare metal stent

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109
Q

ST elevation in leads II, III, and aVF suggest an infarct in which region of the heart

A

inferior (right coronary artery)

you’ll often see bradycardia

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110
Q

which biomarker should you use to look for a re-infarct of myocardium

A

CK-MB

(remember that troponin stays elevated for 7–10 days so it probably wont be helpful info that troponin is elevated…from previous infarct)

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111
Q

a 60 smoker patient has squeezing chest for 30minutes and EMTs give him oxygen and nitroglycerin. BP is 110/70, pulse =90, and ECG is normal. What’s the next step.

A

Give aspirin.

remember that initial ecg and biomarkers can be normal in MI

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112
Q

what ecg leads show the lateral aspect of the heart

A

V5, V6, AVL, I

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113
Q

in heart failure, the renin-angiotensin-aldosterone axis and sympathetic system are activated. These help initially but in the long run make for more cardiac decompensation and remodeling. Heart failure can look like forward failure or backward failure. Describe these.

A

Forward failure: heart isn’t pumping enough blood out so pt has fatigue and lethargy, perhaps even hypotension

Backward failure: increased filling pressures or diastolic dysfunction. Blood backs up–> dyspnea, elevated JVP, perpheral edema, ascites and hepatic congestion

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114
Q

New York Heart Association functional classification of heart failure:

I: no limitation of ordinary physical activity

II: slight limitation of physical activity; develops fatigue or dyspnea c moderate exertion

III: marked limitation, even light activity produces symptoms

IV:__________________

A

NYHA classification IV: symptoms at rest, any activity causes worsening

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115
Q

name major causes of heart failure

A
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116
Q

what drugs have been shown to decrease mortality in HFrEF?

A

ACE-inhibitors*

beta blockers (carvedilol, metropolol, bisoprolol)

*In black pt, use HYDRALAZINE + NITRATES

spironolactone (aldosterone antagonist) can also be used for NYHA class III, IV.

digoxin can be used for symptoms but doesnt affect mortality

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117
Q

why is digoxin used to help relieve symptoms of heart failure

A

digoxin increases heart contractility somewhat

(does not improve survival - for symptomatic relief)

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118
Q

how do nitrates and nitrites help CHF symptoms (note that these aren’t as commonly used although hydralazine + nitrates confere improved survival in black pts)

A

Nitrates reduce preload and clear pulmonary congestion

(remember that’s why we don’t use nitrates for RV infarcts bc the RV is really dependent on preload)

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119
Q

Pts with HFrEF and advanced symptoms may have widened QRS (>120ms), indicating dyssynchronous ventricular contraction. Placement of biventricular pacemaker called………………………………..to stimulate both ventricles simultaneously can reduce symtpoms and imrpvoe mortality

A

Cardiac resynchronization therapy (CRT)

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120
Q

Pts with higher class HFrEF are at increased risk of ventricular arrhythmia and sudden cardiac death. What therapy can be considered?

A

implantable cardiac defibrillator (ICD)

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121
Q

In acute decompensated heart failure, you would treat elevated LV filling pressures with_____________.

You would treat decreased cardiac output with______________ and hypotension with ________________.

A

In acute decompensated heart failure, you would treat elevated LV filling pressures with IV nitroglycerin to decrease preload.

You would treat decreased cardiac output with ionotropes like dobutamine and hypotension with vasoconstrictors like dopamine.

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122
Q

Aortic stenosis is most common symptomatic valvular abnormality in adults. If younger than 30, think congenital bicuspid valve. Pt 30-70, think congenital stenosis or acquired rheumatic heart disease. Older than 70 think calcification. What is the classic *progression* of symptoms of aortic stenosis

A

angina –> syncope –> heart failure

“harsh” systolic murmur

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123
Q

name the three layers of the aortic vessle wall. What predisposes somebody to aortic dissection?

A

intima, media, adventitia. In dissection, there is hematoma in the media that propogates distally. Hypertension is biggest factor in propogation of the hematoma.

cystic degeneration of the media in connective tissue diseases like Marfans and Ehlers-Danlos

hypertension

valve dysfunction like stenois, congenital bicuspid valve

aortic coarctation

pregnancy

athrosclerosis

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124
Q

What do you do for someone with aortic dissection

A
  1. intravenous vasodilator like sodium nitroprusside and introvenous beta blocker like metroprolol or esmolol. Or IV labetalol does both function. Hypertension, shearing forces are what will propogate the dissection so this is most important thing to do.
  2. Noninvasive imaging: TTE (transesophogeal echo), CT or MRI depending on availability. You need to class the AA as Type A (involving ascending aorta) or Type B (not involving ascending aorta)
  3. Type A dissection requires urgent surgery. Type B only requires surgery for complications
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125
Q

Operative repair is indicated for abdominal aortic aneurysms > _____ cm

A

5.5cm or those expanding >0.5cm per year

for smaller aortic aneurysms, serial noninvasive imaging like ultrasound is indicated

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126
Q

A pt presents with severe chest pain radiating to his back, unequal brachial BPs and pulse strengths, and a widened mediastinum on CXR. What do you do next?

A

Get CT. Symptoms consistent with acute aortic dissection.

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127
Q

What defines first degree AV block?

A

prolonged PR interval - longer than 200ms (1 large box)

There is conduction delay in AV node. prognosis is good, usually dont need pacing

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128
Q

CCauses of secondary HTN

A

CHAPSS

Cushings

Hyperthyroidism, hyperaldosteronism

Aorta coarctation

Pheochromocytoma, Polycystic kidney disease

Sleep apnea

Stenosis of renal arteries

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129
Q

what are the initial labs you get for HTN?

A

UA - look for hematuria

urine albumin/creatine spot –check for proteinuria

BMP with calcium and creatinine to check kidney/GFR

Fasting glucose - diabetes

Lipid panel -cvd risk

*base line ECG*

+/- TSH, T4, ECHO, evaluation for 2* causes

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130
Q

Stage II hypertension (what is cut offs) need what kind of pharma therapy

A

Stage II >160/100

Usually need to go ahead and be on 2+ drugs

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131
Q

What antihypertensive drug do you use in pt with diabetic nephropathy or CKD + proteinuria?

A

ACE-i or Arb

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132
Q

SPRINT trial showed that pts 50+ with one or more cardiovascular risk factors had a 30% CVD event risk reduction if BP target was:

A

120 systolic

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133
Q

what are the two common causes of renal artery stenosis?

A
  • Athrosclerosis
  • Fibromuscular dysplasia
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134
Q

bilat flank masses and pain

HTN

hematuria

A

ask about family hx! These are symtpoms of polycystic kidney disease

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135
Q

carcinoid syndrome is caused by overproduction of….

A

serotonin , carcinoid tumors arise in GI tract and lungs

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136
Q

in hypertensive emergency/urgency, don’t lower BP too much…probably 160/100 range.

What are definitions of hypertensive emergency vs hypertensive urgency?

A

Hypternsive urgency: >180/110

Hypertensive emergency: acute elevation in BP with end organ damage

(encephalopathy, MI, aortic dissection, declining renal function, stroke, pulmonary edema from acute LV failure)

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137
Q

tx for hypertensive emergency vs hypertensive urgency

A

Hypertensive emergency: immediate lowering of BP with IV sodium nitroprusside. Lower to 25%/ or 160/110 ish.

*using nitroprusside for multiple days –> cyanide toxicity. May need to use nitroglycerin plus loop diuretics which both reduce preload,

If pt presents with cerebral infarct, don’t lower BP unless systolic >220

Hypertensive emergency: lower BP over few days with oral meds, outpt setting

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138
Q

Pheochromocytomas are usually in medulla of adrenal gland. Test with 24 hr urine VMA, metanephrine, catecholamine. Surgical resection AFTER alpha blockade with phenoxybenzamine.

What are symptoms of pheochromocytoma?

A
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139
Q

what medication must be given before surgical resection of pheochromocytoma?

A

phenoxybenzamine (alpha blocker)

beta blockers may also be given but beta blocker alone will make HTN much worse because alpha adrenergic activity will be unopposed

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140
Q

generally beta blockers are avoided when pt is volume overloaded bc beta blockers reduce cardiac contractility

A

generally beta blockers are avoided when pt is volume overloaded bc beta blockers reduce cardiac contractility

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141
Q

what are two most common causes of afib

A

htn

coronary atherosclerosis

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142
Q

most cases of mitral _____ are due to rheumatic fever worldwide

A

rheumatic fever –> mitral stenosis

opening snap after S2 followed by low pitched diastolic rumble heard best at the apex

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143
Q
A

Wolf Parkinson White (look at delta wave caused by ventricles excited by accessory pathway); pr interval is short, qrs is wide.

Most WPW pts are assymptomatic. Some will get tachy, usually SVT or afib. Afib with WPW looks like ventricular tachy bc of the wide QRS but the irregular irregular rhythm should clue you into afib

for unstable WPW with afib, direct cardioversion

for stable WPW with afib – rate will be really fast bc accessory pathway circumvents sinus pause; beta blockers or CCBs will paradoxically increase rate. Give amiodarone or procainamide

144
Q

what do you give a WPW pt with afib to control rate?

A

amiodarone or afib

(the usual afib rate control agents, bblockers, CCBs paradoxically increase rate bc of that wiley accessory pathway)

145
Q

holosystolic murmur heard at apex, radiating into axilla

A

mitral regurgitation

146
Q

syncope is basically never from TIA bc syncope requires global hypoperfusion and TIA = regional ischemia . What are the only neurological syndromes that *commonly* cause syncope?

A

problems with autonomic nervous system –>orthostatic hypotension–> syncope

  • Diabetes
  • Parkinsons
  • Idiopathic dysautonomia

also sometimes syncope can trigger seizures

147
Q

differential for syncope

A

vasovagal - think about situational eg mictruition

cardiogenic (rhythm v structural)

orthostatic hypotension (20mmHg drop) - usually from meds

carotid sinus hypersensitivity

factitious

148
Q
A

Sick sinus syndrome

sinus bradycardia or arrest/long pause alternates with supraventricular tachycardia, usually afib.

149
Q
A
150
Q

Second degree av block (Wenckebach) (Mobitz I)

A

progressive lengthening of PR interval until beat is dropped – there’s a p wave with no corresponding qrs.

due to abnormal av conduction, may be inferior MI

no need to pace unless symptomatic

151
Q

Describe Mobitz II (2nd degree av block)

A

a dropped beat without prolongation of PR interval

usually a conduction problem in the bundle of His

usually need pacing bc Mobitz II may progress to complete heart block

152
Q

describe third degree AV block

A

SA and AV node are completely doing their own things

atrial rhythm is faster than escape ventricular rhythm

153
Q

treatment for symptomatic or severe bradycardia

A

atropine

154
Q

differential for causes of pericarditis

A

infection: bacterial or viral, TB, parasite

Vasculitis: autoimmune, postradiation

Hypersenstivity/immunologic rxn: eg Dressler

Metabolic: uremia, Gaucher

underlying heart prob eg MI

Trauma

Idiopathic

Neoplasms

155
Q

ECG findings of pericarditis

A

*diffuse* ST elevation

PR depression

(compare to regional ST elevation of MI)

156
Q

How do you tell the difference between acute pericarditis and MI?

It’s really important to get it right bc thrombolytics are right for MI but can lead pericardial hemorrhage and tamponade in pericarditis

A

MI: crescendo pattern of pain, heaviness, squeezing; pain is not worse with respiration!; relief with nitrates. Regional ST elevation with reciprocal ST depression.

pericarditis: sharp pain worse with inspiration, leaning forward helps, nitrates don’t help. Diffuse ST elevation and PR depression

157
Q

LUPUS CRITERIA

  • Malar Rash
  • Discoid Rash
  • Photosensitivity

______________

  • Arthritis
  • Serositis (pleuritis, pericarditis)
  • Renal prob
  • Neuro prob

________________

+ANA

anti dsDNA, anti Smith, antiphospholipid

A

oral, vaginal ulcers

hematologic probs like leukopenia, hemolytic anemia, thrombocytopenia

It’s the renal problems that tend to be most dangerous, most likely to kill a lupus patient

158
Q

Pt with JVD, distant heart sounds, pulsus paradoxus (BP drops on inspiration), dyspnea, chest pain, hypotension

A

pericardial effusion causing cardiac tamponade

ddx: restrictive cardiomyopathy, constrictive pericarditis

159
Q

Beck’s triad

A
160
Q

most common causes of constrictive pericarditis

A

TB

radiation

cardiac surgery

virus

uremia

malignancy

*constrictive pericarditis takes chronic course* Often looks like right sided heart failure (LE edema, hepatomegaly, ascites, Kussmaul sign) + pericardial knock (high pitched early diastolic sound right after S2 (closing of aortic valve)

might need biopsy to differentiate from restrictive cardiomyopathy

161
Q

signs of right sided heart failure

A

Lower limb edema

hepatomegaly

ascites

dyspnea

JVD

Kussmaul sign

162
Q

what is the most common cause of restrictive cardiomyopathy?

A

amyloidosis (an infiltrative disease of the elderly)

(endomyocardial fibrosis w/ eosinophilia is common in developing countries)

163
Q

Of restrictive cardiomyopathy, cardiac tamponade, and constrictive pericarditis, which one(s) show pulsus paradoxus

A

only cardiac tamponade shows pulsus paradoxus out of these

pulsus paradoxus may also be seen in obstructive lung disease

drop in systolic BP with inspiration; if severe, peripheral pulse will disappear during inspiration

tx for cardiac tamponade: pericardiocentesis. While waiting, give IV fluids! Fluid expansion raises preload which they need to keep up cardiac output

tx for constrictive pericarditis: pericardium resection

164
Q

__________________ are the most important step in diagnosis of infective endocarditis

A

serial blood cultures

acutely ill patients should have 3 cx drawn over 2-3 hrs before starting abx

in subacute cases, drawing 3 cx over 24 hours before starting abx is ideal

if pts are critically ill or hemodynamically ill, never wait to start abx. Start empiric treatment and draw blood cx at same time.

165
Q

what bacteria cause infective endocarditis associate with UTI or genitourinary tract instrumentation?

A

enterococci

166
Q

which bacterium in infective endocarditis should prompt a colonoscopy?

A

Streptococcus bovis

167
Q

2 most common organisms that cause infective endocarditis

A

strep viridans (think dental procedures, native valves)

staph aureus (think IV drug users, tricuspid valve endocarditis)

coagulase negative staph –> prosthetic valves

168
Q

Duke Criteria

Major: 1. Isolation of typical organism (strep veridans, s. aureus, HACEK, enterococcus, strep bovis) from 2 blood cx or persistently positive blood cx

  1. Evidence of endocardial involvement (echo, new valve regurg)

Minor: Fever, Immunologic (roth spots, glomerulonephritis, osler nodes, +RF), Predisposing valve situation or IV drug use, +blood cx not meeting major criteria , vascular phenomena (arterial or septic emboli, mycotic aneurysm, Janeway lesions)

How many do you have to meet?

A

2 major

1 major + 3 minor

or 5 minor

169
Q

Duke Criteria

(must meet 2 major, 1 major + 3 minor, or 5 minor)

A

Major: 1. Isolation of typical organism (strep veridans, s. aureus, HACEK, enterococcus, strep bovis) from 2 blood cx or persistently positive blood cx

  1. Evidence of endocardial involvement (echo, new valve regurg)

Minor:

Fever,

Immunologic (roth spots, glomerulonephritis, osler nodes, +RF),

Predisposing valve situation or IV drug use,

+blood cx not meeting major criteria ,

vascular phenomena (arterial or septic emboli, mycotic aneurysm, Janeway lesions)

170
Q

Pt with these lesions, fever and new onset valvular regurgitation

A

most likely infective endocarditis

These are janeway lesions = painless, thought to be caused by septic emboli, occur on palms and soles. A minor criteria (vascular involvement) of Duke criteria.

Get serial blood cultures!!

TEE (transesophageal echo) is imagining of choice

171
Q

what should you always suspect in patient with fever and stroke syndrome?

A

infective endocarditis

172
Q

Patient with fever, new onset murmur, and painful palpable erythematous lesions on pulp of fingers and toes

A

work up for infective endocarditis (serial blood cx and TEE). Osler nodes = immune complex deposition. Roth spots, glomerulonephritis also caused by immune complex deposition in infective endocarditis. Pts might even be +RF!

173
Q

Patient with fever and new onset murmur

A

Work up for infective endocarditis.

These are roth spots, caused by immune complex mediated vasculitis

174
Q

Treatment of Streptococcal endocarditis

A

4-6 weeks penincillin G

if susceptible

175
Q

Treatment of staph endocarditis

A

4-6 weeks of nafcillin, often add gentimycin

if susceptible

(Vancomycin used for MRSA)

176
Q

Treatment for HACEK endocarditis

A

ceftriaxone

177
Q

when is infective endocarditis treated surgically?

A

*usually for infected prosthetic valves

otherwise, CHF that can’t be fixed and is caused by valve failure (a major complication of infective endocarditis), uncontrolled infection, huge vegetation, throwing lotta emboli, no abx treatment, abscesses, etc

178
Q

A pt had prosthetic heart valve within last 6 months and needs dental procedure but is allergic to amoxicillin. What prophylaxis should she get?

A

clindamycin, ampicillin, or cephalosporin will work

179
Q

Peripheral arterial disease workup & management

A

Ankle brachial index (uses doppler us) -normal is slightly above 1, PAD <0.90; Can also do exercise testing

symptomatic pad –>50% 10 year mortality rate! Stop smoking and cut MI risk in half!

supervised graded exercise

tx htn, hyperlipidemia, diabetes, etc.

aspirin, cilostazol

critical limb ischemia, pain at rest, nonhealing ulcers: maybe surgical revascularization

ddx: Takayasu (usually arms, younger women), fibromuscular dysplasia (women), Buerger disease (thromboangiitis obliterans)(smokers)

180
Q

6 P’s of critical limb ischemia: Pain, Pallor, Parasthesia, Pulselessness, Poikilothermia, and (eventually) Paralysis

What is management?

A

In pt with known PAD, think thrombus or embolus (esp if recent procedure, a fib, etc). Give heparin to stop thrombus from propagating. Put limb below horizontal plane with no pressure. Artiography to identify occlusion and then surgical intervention.

181
Q

virchow’s triad

A
182
Q

Name 2 most common inherited hypercoagulobility problems

A

Factor V Leiden

Prothrombin mutation

183
Q

The usual cause of death from pulmonary embolism is…

A

progressive right heart failure from pulomonary HTN

184
Q

acute onset of hypoxemia in pt with normal CXR should be interpreted as _____ until proven otherwise

A

PE

185
Q

wells criteria

A

PE unlikely? d dimer to rule out

PE likely? get chest ct with contrast

186
Q

Management of PE

A
  • Pts with severe problems, rt heart failure, hypotension, get rid of the current clot: surgical removal of clot or tPA if systolic bp<90 mmHg.
  • Pts who are stable: goal becomes prevent future clots.

Start with Unfractionated Heparin, Low Molecular Weight Heparin or Fondaparinux. LMWH and fondaparinux have rapid onset, predicatble does response and don’t require constant lab monitoring like unfractionated heparin.

Bridge to Warfarin: Use LMWH or fondaparinux for at least 5 days while overlapping warfarin with at least 2 consecutive days at therapeutic INR ~2.5

or IVC filter

187
Q

how many posterior ribs on inspiratory cxr?

A

8-10 posterior ribs (the horizontal ones)

188
Q

2 drug classes of bronchodilator

A

anticholinergic

beta agonist

189
Q

tachypnea = ___ breaths per min

A

>40

190
Q

treatment for COPD exacerbations

A

bronchodilators (beta agonists, anticholinergics)

oxygen

glucocorticoids

abx if infection suspected

191
Q

5 h’s of asystole and PEA

A

Hypovolemia

H+, acidosis

Hypoxemia

Hyperkalemia

Hypothermia

192
Q

5 t’s of PEA, asystole

A

Trauma

Tamponade

Tension pneumothorax

Toxins

Thrombosis (heart–> MI, or PE)

193
Q

painless thyroiditis

A

brief hyperthyroid state but low radio iodine uptake

+TPO antibody

painless, small goiter

spontaneous recovery

194
Q

tx for CO poisoning

A

100% O2 non rebreather mask

195
Q

hepatic transaminase levels in alcoholic hepatitis

A

elevated AST, ALT but rarely >500

AST:ALT 2:1

196
Q

Name 3 symptoms of chronic pancreatitis

A

malabsorption (steatorhea, weight loss)

chronic epigastric pain with intermittent pain free periods (radiates to back, not improved with antacids, maybe helped by sitting up and leaning forward)

diabetes mellitus

Get CT look for calcifications

197
Q

treatment for chronic pancreatitis

A

alcohol and smoking cessation

pain control

small frequent meals

enzyme replacement

198
Q

differential for syncope

A

cardiogenic: LV outflow obstruction, conduction problem, Vtachy
vasovagal: prodrome?

autonomic dysfunction

hypovolemia

carotid hypersensitivity

199
Q

How does acetaminophen affect warfarin?

A

tylenol potentiates warfarin

remember that vit K is antidote but takes 12-24hrs so give prothrombin complex concentrate (if available) or fresh frozen plasma if not for faster clotting

200
Q

diagnostic tests for heart failure

A

BNP (right atrial stretch)

ECHO

left heart cath -tells you if ischemic or not

(you’ll prob do ecg which doesnt diagnose hf but might give clues about etiology)

201
Q

HF treatment

A

everyone gets ACEi/Arb, and beta blocker, H2O and Na restriction. If ischemic: statin + asparin

if symptomatic: furosemide

if class III: isosorbidedinitrate hydralazine/spironolactone

if EF<35% and NOT class iv (no symptoms at rest) then they get defibrillator

class IV: inotropes, will die in a year;

202
Q

Approach to HF exacerbation

A

Get CXR, ECG, troponin, BNP

if STEMI –> Mona bash and cath

if just CHF: LMNOP

lasix, morphine, nitrates, oxygen, position

203
Q

symptoms of salicylate overdose

A

tinnitus, tachypnea, fever, GI probs, nausea

*mixed acid base disturbance (respiratory alkalosis + metabolic acidosis = near normal pH)

-Salicylate OD is indication for hemodialysis

204
Q

describe acid/base disturbance of salicylate overdose

A

First aspirin overdose causes respiratory alkalosis by causing tachypnea –> blow off CO2 (acid) low pCO2

Then aspirin uncouples oxidative phosphorylation, leading to accumulation of acids like lactic acid and pyruvic acid –> anion gap acidosis which sucks up all the bicarb low bicarb

205
Q

Indications for hemodialysis

A

AEIOU

Acidosis (<7.1)

Electrolytes (refractory hyperkalemia)

Intoxications

Overload refractory to diuresis

Uremia

206
Q

metformin can cause …… deficiency

A

B12

gait problems , + babinski , parasthesias, neuropsychiatric changes.

207
Q

metabolic acidosis

___ bicarb

A

low pH, low bicarb

Check anion gap

208
Q

cosyntropin test is for….

A

primary adrenal insufficiency

209
Q

tx for vasospastic angina

A

calcium channel blocker

210
Q

tx for female pattern hair loss

A

topical minoxidil

211
Q

causes of hyperandrogenism in women

A

PCOS

neoplasm (esp if rapid change)

hyperprolactinemia

Cushing

nonclassic congenital adrenal hyperplasia

acromegaly

212
Q

These hands in setting of chronic hep C

A

porphyria cutanea tarda

also seen in hemochromotosis, alcohol, estrogen use

213
Q

primary sclerosing cholangitis

pathophys?

association with what disease?

A

chronic inflammation of intra and extra hepatic ducts

ulcerative cholitis

increase in conjugated bilirubin, pANCA

214
Q

chest pain + segmental ischemic changes on ECG in post menopausal woman –> cath shows no occlusion. What’s going on?

A

Ask about recent stressors. Could be broken heart syndrome. segmental ischemic changes . probably due to catecholamine surge. tx is supportive usually self resolves

215
Q

Antibiotics for MRSA

A

Sulfamethoxazole/trimethoprim

Doxycycline

Clindamycin

Linezolid

Vancomycin

Daptomycin

216
Q

antibiotics contraindicated in pregnancy

A

MCAT

metronidazole

chloramphenicol

aminoglycoside (streptomycin, gentomycin, tobramycin)

tetracycline

217
Q

name 4 antibiotics with pseudomonas activity

A

ciprofloxacin

Zosyn (piperacillin, tazobactim)

cefepime

levofloxacin

azetreonam

218
Q

VRE antibiotics

A

linezolid

tedizolid

daptomycin

tigecycline

and more

219
Q
A
220
Q
A
221
Q

immunosuppressant drug that might cause hyperkalemia, gout attacks, tremor, htn

A

tacrolimus

222
Q

what kind of drug is azathioprine?

A

immunosuppressant. stops purine synthesis–> leukocyte production

bone marrow suppression : (

hepatoxicity : (

223
Q

lupus nephritis is caused by deposition of…

A

anti double stand DNA–> complement mediated damage

lupus nephritis kinda mixed pic of nephritic/nephrotic –

224
Q

normal arterial pH and paCO2 in context of increased work of breathing indicates what…

A

that the pt is wearing out and can’t maintain adequate ventilation (either muscle fatigue or air trapping) and points to impending respiratory collapse

for example: pt with acute asthma attack is expected to have respiratory alkalosis with low PaCO2 due to hyperventilation. Normal or elevated PaCO2 during acute asthma attack is bad bad!

225
Q

bactrim side effects

A

pancytopenia

nausea/vomiting

rash

hyperkalemia

interacts with warfarin

226
Q

lower extremity weakness, pain swelling after drinking binge

A

acute alcohol myopathy

watch out for rhabdo

cocaine can also cause rhabdo

227
Q

what drugs can cause rhabdomyelosis

A

-things that will make you pass out so much you dont move: benzos, etoh, opioids

statins

cocaine, alcohol, meth

colchinine

228
Q

tx for rhabdo

A

IVF

(watch out for compartment syndrome)

229
Q

how do you treat mycobacterium avium complex

A

MAC happens in aids pts with t cell count below 50

tx with macrolide +ethambutal

symptoms are diarrhea, fever, abdominal pain, hepatosplenomegaly , high alkphos

230
Q

name 3 macrolids

A

azithromycin

clarithromycin

erythromycin

231
Q
A
232
Q

difference between secretory and osmotic diarrhea

A

osmotic diarrhea is because of nonabsorbed, osmotically active solute. High stool osmotic gap (290-2(Na +K)). Occurs after ingestion.

Secretory diarrhea can happen without eating. The gut secretes electrolytes and the osmotic gap is low.

-toxins, absorption issues, hormones (VIPomas). post surgery, CF, Vibreo cholerae

233
Q

sepsis is common cause of mixed respiratory acidosis and metabolic acidosis

A

sepsis –> metabolic acidosis, requires compensatory respiratory alkalosis but muscles fatigue and you cant blow off CO2 as you approach respiratory failure leading to respiratory acidosis . look for really low pH

234
Q

SIRS criteria

A

Temp: below 96.8 or above 100.4

HR: >90bpm

Tachypnea: >20 RR

WBCs: <4000, >12000, or bandemia

235
Q

what are major signs/symptoms of sepsis

A

think about it by organ system

brain– AMS

kidney – BUN:Cr

cardiovas - hypotension

liver – LFTs

lung – CXR (maybe ARDS)

236
Q

what’s difference between sepsis, severe sepsis, and septic shock

A

all SIRS 2/4 positive

severe sepsis: >= 1 organ system dysfunction; responsive to fluids

septic shock: >= 1 organ system dysfuntion, NOT responsive to fluids, will need vasopressors

237
Q

BUN: creatinine ratio in ATN

A

10-15

238
Q

pt with neck stiffness, a cranial nerve palsy, weeks of headache and malaise. CSF shows low glucose, moderately increased protein, and lymphocytosis

A

tuburcular meningitis

239
Q

febrile neutropenia

A

a medical emergency

need anti-pseudomonal coverage; antipseudomonal beta lactam (cefepim, meropenem, piperacillin-tazobactam) will cover gram pos and gram neg

240
Q

vancomycin has no ______ activity

A

gram negative

vancomycin used known MRSA, cather related infection, soft tissue, skin, pneumonia, hemodynamic instability

241
Q

mild fever, pulmonary symptoms,

A

blastomycosis

midwest USA

can become disseminated even in immunocompetent

itraconazole or amphotericin B if really severe

242
Q

cerebellar degeneration is associated with what common medical problem

A

alcohol use disorder

heavy alcohol use can cause cerebellar neurotoxicity – wide based gait, postural instability; cognition generally intact

243
Q

triad of Wernicke encephalopathy

A

ocular motor dysfunction (horizontal nystagmus)

**confusion (differentiates it from alcohol neurotoxicity in cerebellum(

ataxia

244
Q

risk of giving oxygen during COPD exacerbation

A

hypercapnia—> acidosis and vasodilation–>confusion, lethargy, seizures

Giving the oxygen will help the hypoxemia but it won’t help and may even worsen CO2 trapping in advanced COPD.

O2 may exacerbate CO2 trapping by reducing respiratory drive, loss of compensatory vasoconstriction in regions of lung where there is ineffective gas exchange; more oxyhemoglobin decreases CO2 uptake from the tissues by Haldane effect

Goal is to get to sat in low 90s

245
Q

antimitochondrial antibody is associated wth

A

primary biliary cholangitis

cholestasis with intrahepatic autoimmune bile duct destruction

think middle aged women

ursodeoxycholic acid

many pts wind up needing liver transplant

elevated alkphos

246
Q

what baseline test should pt getting traztuzamab for HER2+ breast cancer get?

A

baseline ECHO

traztuzamab is cardiotoxic

247
Q

anastrozole and letrozole used for postmenopausal estrogen receptor + breast cancer.

What side effect should you be most worried about with anastrozole and letrozole (aromatast inhibitor)

A

decreased bone density

248
Q

HIV predisposes pts to malignancy because T cells arent as able to target mutated cells for apoptosis and latent oncogenic viruses reactivate.

Name 3 virus-malignancy combos seen in HIV/AIDS

A

Epstein Barr Virus –> diffuse large B cell lymphoma, CNS lymphoma (non hodgkin lymphoma). Diffuse lymphadenopathy + B symptoms

HHSV 8 –> Kaposi sarcoma

HPV–> invasive cervical carcinoma

249
Q

tick born illnesses

A

Rocky mountain spotted fever - rash on palms, soles;

Erlichiosis - leukopenia, thrombocytopenia

babeiosis - northeast, hemolytic anemia , thrombocytopenia, esp in older/immunocomp/asplenic ppl

250
Q

heart failure in an alcoholic

A

alcoholic cardiomyopathy

dilated cardiomyopathy; LV function returns with abstinance

251
Q

Jarish herxheimer reaction

A

from sudden lysis of spirochetes (syphilis, lyme)

myalgias, fever, chills

self limited

252
Q

treatment for arsenic poisoning

A

dimercaprol

253
Q

chronic arsenic poisoning symptoms

A

hyper/hypo pigmentation, hyperkeratosis, stocking glove neuropathy

254
Q

encephalopathy + ataxia + eye dysfunction

A

wernicke’s encephalopathy, give thiamine

255
Q

This in HIV patient without eye pain

A

CMV retinitis. Note the fluffiness.

256
Q

liraglutide

A

GLP-1 agonist

weightloss

decreased CVD mortality

257
Q

Old man with ESRD, back pain, normal calcium, high phosphate, high alkphos

1 what would you think it is if Xray shows mixed osteoblastic/osteolytic lesions in spine?

2 what would you think if his Xray shows widespread osteopenia and subperiosteal bone resorption in spine

3 what would you think it is if his xray shows irregular area of bone sclerosis in spine?

A
  1. normal calcium, high alkphos (not high phosphate) with mixed osteoblastic/osteolytic lesions –> Paget’s disease of the bone. Usually asymptomatic
  2. Phosphate will be high in ESRD. people with kidney failure get hyperparathyroidism bc of low calcium/high phosphate –> bone resorption called renal osteodystrophy
  3. Irregular bone sclerosis (osteoBLASTIC) and progressive back pain should make you think mets, probably prostate mets
258
Q

Formula to correct calcium for albumin

A

=Ca +0.8 (4-albumin)

259
Q

citrate in massive blood transfusions binds to…. causing low serum levels

A

massive blood transfusions –> hypocalcemia bc citrate binds to Ca2+

260
Q

2 main factors in calcium regulation

A

parathyroid hormone (adjust calcium minute to minute)

and vitamin D (adjusts calcium over long term)

261
Q

Hepatorenal syndrome

A

a complication of liver failure, often set off by peritonitis, excessive diuresis, GI bleed, other major insult

as cirrhosis progresses, the splenchnic artery dilates and there is less vascular resistance. This activates RAAS –> renal vasoconstriction and therefore decreased perfusion and GFR. acute tubular necrosis or other AKI should be on your differential but HRS patients won’t get better with fluids and they will have bland U/A.

treatment = liver transplant

262
Q

Lights criteria

A

pleural fluid protein/serum protein >0.5

pleural fluid LDH/serum LDH >0.6

pleural fluid LDH > 2/3 upper limit of normal LDH

263
Q

most common causes of bloody plural effusion

A

trauma

malignancy

PE

264
Q

Horner syndrome

A

Ptosis

Miosis

Anhidrosis

associated with apical lung cancer (Pancoast tumor)

265
Q

hemoptysis with blood streaked purulent sputum

A

Think bronchitis

266
Q

chronically coughing up copious sputum

A

bronchiectasis

267
Q

hemoptysis with acute onset of pleuritic chest pain and dyspnea

A

pulmonary embolism

268
Q

paraneoplastic syndromes associated with small cell lung cancer

A

SIADH

cushings (ACTH)

269
Q

CMV in immunocompromised person causes what symptoms

A

pneumonitis

gastroenteritis

hepatitis

270
Q

vitamen D deficiency –>low calcium –> parathyroid hormone released and bone resorbed. Maybe bone pain, osteomalacia. If kidneys work, phosphate will be low and calcium will return to normal or slightly low

A
271
Q

whats the mechanism of warfarin skin necrosis

A

warfarin lowers protein C first before the results of its inhibition of production of II, VII, IX, X –> transient hypercoagulable state –> VTE or skin necrosis especially in people who have hereditary protein C deficiency

TX: stop warfarin, give protein C concentrate

272
Q

main 2 lung infections for immunocompromised pts

A

CMV (diarrhea too)

P. jirovecii

Prophylaxis: TMP-SMX, ganciclovir

273
Q

severely elevated triglyceride levels (>1000) can cause…

A

pancreatitis!

give fibrates, fish oil, no alcohol

274
Q

brown sequard syndrome

A
275
Q

TTP is the story of ADAM and the FAT (RN)

A

ADAMTS-13

Fever

Anemia (hemolytic)

Thrombocytopenia

+/-Renal failure

+/- Neuro sx

platlets low + schistocytes on smear but PT/PTT, fibrinogen and D-dimer normal

276
Q

Lab findings in DIC

A

low platelets

schistocytes on smear

high PT PTT

high D dimer

low fibrinogen

277
Q

Heparin Induced Thrombocytopenia

A

7-14 days after heparin product started; antibodies to platelet

tx: stop heparin, start argatroban and bridge to warfarin

278
Q

immune thrombocyopenia

A

antibodies to plt in women with autoimmune disorder

tx with steroids, IVIG

if that doesn’t work: splenectomy

if that doesnt work: rituximab

279
Q

what marker is elevated in polymyositis (not antibody)? what’s treatment?

A

creatinine kinase is elevated in polymyositis and NOT in polymyalgia rheumatica

+ANA, +anti-Jo

280
Q

furosomide cause hypo______ and hypo______

A

hypokalemia

hypomagnesium

281
Q

what arrythmia does digitalis cause

A

atrial tachycardia with av block

282
Q

giardia treatment

A

metronidazole

283
Q

methotrexate side effect

A

impaired DNA synthesis–> seen in most rapidly dividing cells like oral mucosa (stomatitis, oral ulcers) and bone marrow (MACROCYTIC anemia

methotrexate also causes hepatotoxicity

all this can be avoided by giving folic acid along with methotrexate

284
Q

Hep C with palpable purpura

A

cryoglobinemia

if severe: plasma xchange; steroids, cyclophosphamide

285
Q

palpable purpura plus GI symptoms

A

henloch scholein purpura

biopsy

steroids

286
Q

Pt with hemoptysis and hematuria—> what 2 weird disease should be in differential

A

Goodpasture and Wegners (granulomatous polyangiits)

Wegners has weird nose stuff, C-ANCA

287
Q

granulomatous polyangiitis

antibody?

tx?

A

hemoptysis, hematuria, nose stuff

cANCA

steroid, cyclophosphamide

288
Q

pt with Hep B + gut, renal and skin problems, maybe weird nerve stuff

A

polyarteritis nodosa!

get angiogram

steroids, cyclophosphamide

289
Q

What test do you do for Wilsons?

A

1st: Slit Lamp

cerruplasm

urinary copper

gold: biopsy
tx: penacillamine, transplant

290
Q

Wilson’s disease treatment

A

penacillamine, transplant

(Kaiser-Fleicher rings in eyes, cirrhosis, chorea from copper in basal ganglia)

291
Q

hemochromatosis symptoms

A

Bronze diabetes

cirrhosis

diastolic CHF

test: ferritin >1000 or transfarrin saturation >50% or biopsy or gene mutation

blood letting

undo the iron from me: deferoxamine

292
Q

primary symptoms of alpha one tripsan deficiency

test

A

COPD + cirrhosis in young person

biopsy and look for PAS + macrophage

293
Q

dry cough, African american, hilar lymphadenopathy, hypercalcemia

A

sarcoidosis

also arthralgias, eye stuff, tender nodules –> granulomatous

294
Q

PBC labs show increased alk phos, increased conjugated bilirubin.

What disease often co occurs with Primary biliary cholangitis?

A

osteoporosis

295
Q

most common malignancy in people with asbestosis

A

bronchogenic carcinoma

296
Q

what lung cancer can cause cavitary lesions?

A

squamous cell

297
Q

hypercoagulobility + diarrhea

A

pancreatic cancer

298
Q

signs of beta blocker overdose

A

cardiogenic shock

also stop endogenous catecholamines from stimulating glycogen breakdown –> hypoglycemia

give IVF, atropine, glucagon

299
Q

methotrexate adverse side effects

A

hepatoxicity

cytopenias (give folate)

methotrexate is dmard for RA

300
Q

hydroxychloroquine adverse effects

A

retinopathy

hydroxycholorquine is a TNF and IL-1 suppresor

301
Q

chondrocalcinosis on xray of a joint associated with pseudogout. What are 3 conditions that increase chance of pseudogout

A

hyperparathyroidism

hypothyroidism

hemochromotosis

302
Q

tolterodine

A

anticholinergic for urge incontinence and overactive bladder

303
Q

hypercalcemia, renal dysfunction, anemia, back pain, infections

A

think multiple myeloma

hypercalcemia + anemia from bone marrow infiltration. hypercalcemia can cause constiption, depression, fractures

malignancy of plasma cells

304
Q

tests for multiple myeloma

A

serum/urine protein electrophoresis (look for M spike) (have to do urine to look for light chains)

blood smear (rouleux)

bone marrow biopsy

305
Q

how to calculate number needed to treat

A

NNT = 1/ (control rate of disease - treatment rate of disease)

for example, if 75% of control group have the event but 60% of treatment group have the event then

NNT = 1/(.75-.6)

= 7

306
Q

hemi neglect is caused by stroke where…

A

contralateral PARIETAL lobe

307
Q

euvolemic hyponatremia associated with…

A

SIADH

think small cell lung cancer, pituitary prob

-water restriction, maybe a salt tablet

giving isotonic fluid like NS or LR may make the problem worse bc patient will retain more water…further dilution of the sodium they have…worse hyponatremia which can lead to confusion, seizures, coma

308
Q

cirrhotics have lower temperatures so temp doesnt have to be as high, just >100, to suspect spontaneous bacterial peritonitis if they have ascites

A
309
Q

abdominal pain

+ upper limb neuropathy

+ positive urine urobilinogen

A

acute intermittent porphyria

port wine colored urine

it’s an autosomal dominant problem in heme synthesis. the built up precursors are neurotoxic so all the symptoms are from neuro probs but you get abdominal pain that is from neuropathy. +/- neuropsychiatric manifestations +/- autonomic dysfunction. You can also get SIADH –> hyponatremia.

Tx: glucose + hemin (heme analogue)

310
Q

side effects of isoniazid

A

neuropathy from pyridoxine deficiency (B6). isoniazid causes B6 excretion and most people don’t have a problem bc they have a big B6 store. But pts with diabetes, malnutrition, pregnancy may not have enough B6 –> peripheral neuropathy esp vibratory sense loss.

also isoniazid causes hepatotoxicity

311
Q

huntington disease causes loss of what kind of neuron?

A

GABA-ergic

caudate nucleus and putamen atrophy

312
Q

abdominal pain and bloody diarrhea after eating undercooked meat

A

cambylobacter or EHEC

313
Q

bloody diarrhea, often with bacteremia, associated with contaminated water or food, especially from travel outside US

A

Shigella

*can cause HUS (hemolysis, renal failure)

314
Q

vomiting, diarrhea, abdominal pain after undercooked shellfish

A

Vibreo fulnificus

**really a problem for immunocompromised. immunocompromised should not eat raw oysters

315
Q

colon ca chemo

A

FOLFOX/FOLOFIRI

plus vegf-inhibitor bavacizumab

316
Q

freckled mouth…look for what cancer?

A

small bowel with endoscopy

peutz jager

317
Q

Lynch syndrome cancers

A

Colorectal

Endometrial

Ovarian

(Merrill lynch was a ceo)

aka hereditary nonpolyposis colorectal cancer

defect in DNA mismatch repair

3-2-1 rule: 3 cancers, 2 generations, 1 younger than should have been

318
Q

APC gene mutation causes…

A

familial adenomatous polyposis

1000s of polyps by teens

must do prophylactic colectomy

319
Q

Turcas

think turban…brain cancer plus what other cancer?

A

colorectal

320
Q

Gardners

A

jaw cancer and colorectal ca

321
Q

progression of pertusis

A

stepwise

weeks 1-2 mild cough + rhinitis

weeks 2-6 the badness

convalescence weeks to months, gradual improvement

tx with macrolides

*lymphocyte predominant leukocytosis

322
Q

signs of hyperparathyroidism

A

kidney stones (calcium); high blood and urine calcium

323
Q

what neoplasm is mysthenia gravis associated with

A

thymoma

324
Q

neoplasm associated with H. pylori

A

MALT lymphoma

325
Q

metoclopromide is a ________antagonist and can cause ___________ symptoms

A

metoclopromide is a dopamine antagonist and can cause extrapyramidal symptoms

like acute dystonia (think neck probs), parkinsonism, akathisia

326
Q

when treating for Clostridum septicum bacterima, what underlying condition should you rule out?

A

colon cancer

the tumors make C. speticum happy enough to create spores plus the tumor disrupts the gut/blood barrier so those spores can get into the blood

327
Q

nephrotic syndrome can cause accelerated _________ and a _________________ state

A

nephrotic syndrome can cause accelerated athrosclerosis and a hypercoagulability state

328
Q

which part of spinal cord is hurt when there is motor weakness, loss of pain and temperature but preservation of position and vibration

A

anterior spinal cord, usually from an injury to anterior spinal artery

329
Q

UTI or pylo + alkaline urine should raise suspicion for which organisms

A

Proteus mirabilis (more common)

Klebsiella pneumonia

alkaline urine can cause struvite stones (magnesium ammonium phosphate)

330
Q

name some causes of stephen johnson syndrome/toxic epidermal necrosis

A

mycoplasma pneumonia

TMP-SMX, other abx

anticonvulsants (phenytoin, lamotrigine, carbamezapine)

NSAIDs

allopurinol

sulfasalazine

vaccination

graft-vs-host

SJS <10% of body, TEN > 30%

331
Q

treatment for rosacea

A

topical metronidazole

332
Q

treatment for cholangitis

A

cipro + metronidazole

333
Q

treatment for pyelo in someone nontoxic

A

cipro

334
Q

tx for pyelo in someone really sick

A

ceftriaxone

335
Q

tx for CAP

A

azithromycin and ceftriaxone

336
Q

tx for diverticulitis

A

Cipro (G-) + metronidazole (anaerobes)

337
Q

tx for hospital acquired pneumonia

A

vanc + pip/tazo

338
Q

uncomplicated UTI tx

A

TMP-SMX

nitrofurantoin

339
Q

if you find medullary thyroid cancer in a patient (elevated calcitonin), what test should you get next?

A

plasma fractionated metanephrine

to check for pheochromocytoma

as part of MEN2A

340
Q

tests for cushings

A

low dose dexomethasone suppression

salivary cortisol

341
Q

MEN type 1

A

primary hyperparathyroidism (increased calcium)

pituitary tumors

pancreatic tumors (esp gastrinomas)

342
Q

antibody in granulomatosis with polyangitiis

A

c-ANCA

343
Q

huntington’s affects what part of brain

A

caudate nucleus and putamen

344
Q

polyarteritis nodosa

A

asymmetric polyneuropathy

livedo reticularis

kidney problems

ischemia and perforation in Gut

ANCA NEGATIVE

constitutional symptoms, high inflammatory markers

due to transmural inflammation of medium arteries

** Associated with Hepatitis B/C **

345
Q

which TB drug causes hepatoxicity

A

isoniazid

346
Q

don’t ever give ACEi to ….pts

A

cirrhosis

(RAAS important for counteracting splanchnic dilation and preventing hypotension)

347
Q

low levels of what hormone can lead to SIADH?

A

cortisol

348
Q

what kind of diarrhea happens at night

A

secratory

(VIPoma (in pancreas with flushing), gastrinoma, chronic infection, microscopic colitis, bile salt diarrhea

349
Q

erlichiosis

A

no rash, fever myalgia confusion

low platelets low leukocytes

empiric doxy

350
Q

what lung cancer causes cavitary lesions

A

squamous cell (most common among smokes)

squamous cell can cause PTHrp too

351
Q

enterotoxin made in intestine …>1 day to onset….which bugs?

A

C diff

ETEC

Vibrio cholerae

352
Q

s bovis is now known as

A

s gallolyticas

colon cancer!

353
Q

3 major thangs of milk alkali syndrome

A

acute kidney injury

hypercalcemia

metabolic alkalosis

354
Q

SAAG

A

serum albumin - ascites albumin

>1.1 cirrhosis, cardiac ascites, budd chiari

<1.1 TB, pancreatic cause, nephrotic syndrome, peritoneal carcinomatosis

355
Q

consensus trial showed acei can reduce moratality for HF but ARNIs better apparently . Acei better than arb

A

internal medicine nbme shelf (2 decks)

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