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A - Step II > Medicine GI, CV, Fem/M-Rep, Heme Onc, Pulm, Ren, NS > Flashcards

Medicine GI, CV, Fem/M-Rep, Heme Onc, Pulm, Ren, NS Flashcards

1
Q

Pt with recurrent episodes of pneumonia, sinusitis, and GI infections should make you think of? What test should you get to establish the diagnosis?

A

humoral immunity defect -> get serum Ig to establish a diagnosis

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2
Q

renal vein thrombosis is commonly associated with which nephrotic syndrome?

how does it present?

A

membranous glomerulopathy

presents with typical nephrotic syndrome features caused by hypoalbuminemia: periorbital edema, abdominal disteinsion/ascites, lower extremity edema, proteinuria

renal vein thrombosis: acute onset of abdominal pain, fever, and hematuria

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3
Q

2 major side effects of statins

A

rhabdomyolysis, can lead to renal failure

slightly elevated transminases

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4
Q

most rapid way to decrease serum K concentration (2)

A

insulin (effect usually occurs within 15-30min) + glucose to avoid hypoglycemia

K can be shifted intracellularly more quickly than it can be removed from the body. However, because this effect is transient, efforts to decrease the total body K should still be made via

Kayexalate (1-2hrs)

furosemide

ß2 agonist

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5
Q

Rx that have been shown to confer a survival benefit in CHF

A

ACEi

ARB

ß-blockers

spironolactone

“SAAB”

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6
Q

most common cause of CKD and ESRD requiring dialysis

A

diabetes

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7
Q

why and when does diabetic nephropathy usually occur?

what other symptoms do patients usually present with?

A

10-15 years after the onset of type I/II DM

occurs because advanced glycation end products and other inflammatory mediators damage the glomerulus, resulting in proteinuria, glomerular nephropathy, and ESRD

at this point, patients typically have 3+ protein, elevated creatinine, decreased visual acuity, elevated BP, and no active urinary sediment (red/cellular casts) to indicate a different etiology of the proteinuria

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8
Q

What is the PVR in a patient with significant bladder outlet obstruction (ie BPH)?

A

>50 cc

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9
Q

2 coronary vasodilators

A

dipyridamole and adenosine

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10
Q

what is the coronary steal phenomenon? What medications are usually employed to test this and what is it used to test for?

A

dipyridamole & adenosine - coronary vasodilators

CPS - in patients with CAD, the diseased vessels distal to the obstruction are maximally dilated (ie their ability to increase myocardial perfusion is limited). Thus as the non-diseased vessels are dilated by these medications, there is a redistribution of coronary blood flow to non-diseased areas, resulting in diminished perfusion of the diseased segments

used to diagnose ischemic heart disease

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11
Q

Patient w/ UC presents with 6 mo history of fatigue and pruritis.

Albumin 3.8

Tbili 1.7 (slightly elevated)

Alk Phos 816 (elevated)

AST 45 (WNL)

ALT 54 (WNL)

ESR 102 (high)

pANCA (+)

What is your leading diagnosis? How would you confirm it?

Other common presenting symptoms?

A

Primary sclerosing cholangitis

diagnose with cholangiogram (ERCP or MRCP) - shows multi-focal narrowing with intra-hepatic and extra-hepatic duct dilation

other symptoms are releated to cholestasis - fatigue, pruritis, steatorrhea, fat soluble vitamin deficiencies, metabolic bone disease, hepatic failure

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12
Q

metabolic and electrolyte changes in a patient with bulimia nervosa

treatment and justification of treatment?

A

chronic vomiting -> volume depletion + HCl loss ->

metabolic alkalosis

hypoklaemia

hypochloremia

trmt: normal saline - restores arterial volume, correct hypochloremia, and increases urinary bicarb excretion

note that metabolic acidosis consists of 2 phases: generation phase (excess bicarb produced) + maintenance phase (process preventing renal bicarb excretion)

  • generation phase - due to urinary or GI H+ losses (diuretics, vomiting) or decreased PO intake
  • maintenance phase - due to hypovolemia, kidneys perceive decreased effective circulating volume and results in RAAS activation -> reabsorption of Na, K, excretion of H, decreased excretion of bicarb
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13
Q

physiology of metabolic acidosis secondary to an underlying disorder

treatment?

A

consists of 2 phases: generation phase (excess bicarb produced) + maintenance phase (process preventing renal bicarb excretion)

generation phase - due to urinary or GI H+ losses (diuretics, vomiting) or decreased PO intake

maintenance phase - due to hypovolemia, kidneys perceive decreased effective circulating volume and results in RAAS activation -> reabsorption of Na, K, excretion of H, decreased excretion of bicarb

trmt: normal saline to restore arterial volume, correct hypochloremia, and increases urinary bicarb excretion

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14
Q

rapid association: systolic-diastolic abdominal bruit in a patient with HTN and atherosclerotic disease

A

renal artery stenosis

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15
Q

rapid association: patient with history of HTN has a medication list that includes lisinopril, HCTZ, amlodipine, metoprolol, aspirin, metformin, and glyburide; current BP is 190/120

A

renal artery stenosis - note that his BP is still high despite the use of multiple medications

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16
Q

What is SAAG?

What are the implications of this value?

A

serum-to-ascites albumin gradient

(calculate by substracting peritoneal fluid albumin conc. from serum albumin conc.)

used to assess ascitic fluid to diagnose the etiology

SAAG > 1.1 = portal HTN/cardiac ascites/increased hydrostatic pressures within hepatic capillary beds

SAAG < 1.1 = other etiologies (malignancy, pancreatitis, nephrotic syndrome, tb)

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17
Q

pt presents with fatigue, dark urine; PE shows icteric sclera and skin. Labs shows elevated AlkPhos.

Next best step in management?

A

get US

elevated alkphos are indicative of cholestasis and these patients should be elevated with an RUQ US to assess for intra- vs extra- hepatic causes of biliary obstruction

(+) biliary dilation -> extrahepatic cholestasis

(-) biliary dilation -> intrahepatic cholestasis

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18
Q

when a patient presents with weight loss, blood in stools, and has a family history of colon cancer, aside from the w/o for colon cancer, what else should the patient be evaluated for?

A

endometrial cancers.

Why? She has Lynch syndrome (aka HNPCC), and Lynch II is associated with a high risk of extracolonic tumors, the most common of which is endometrial carcinoma, which develops in 43% of females in affected families

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19
Q

Best imaging modality for assessing patients with an acute episode of diverticulitis

A

CT scan

However, if you suspect a perforation secondary to diverticulitis, an upright xray may be employed to look for free air under the diaphragm

AVOID colonoscop/sigmoidoscopy during an acute episode, as the endoscope can perforate the fragile bowel and lead to massive contamination of the abdominal cavity with fecal material

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20
Q

3 major cardiac causes of arterial emboli

A

LV thrombus, usually secondary to recent STEMi

atrial thrombus secondary to a-fib

aortic atherosclerosis

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21
Q

most common complication of PUD and how does it present?

A

hemorrhage - presents as hematemesis +/- melena, though a massive upper Gi bleed may present as hematochezia (usually a sign of lower GI bleed)

other complications: perforation, penetration, obstruction

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22
Q

pre-test probability of coronary artery disease is based on several factors. What dictates a low-risk patient?

These patients typically undergo a stress test, which can be positive or negative. How would you interpret either one?

A

low-risk: men <40/women <50 with atypical chest pain and ø significant cardiac risk factors (non-smoker, no family hx of premature CAD)

(+) stress test in patients at low-risk for CAD -> likely to be a faslse (+)

(-) stress test in patients at high-risk for CAD -> likely to be a faslse (-)

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23
Q

Hep C is a risk factor for these diseases

A

cirrhosis

HCC

cryoglobulinemia

glomerulonephritis

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24
Q

What is a parapneumonic effusion and what are they typically caused by?

What are the different types and how are they managed?

A

type of pleural effusion that arises as a result of apneumonia, lung abscess, or bronchiectasis; can be either

  • uncomplicated - exudative (predominately PMNs) effusions secondary to inflammation associated with pneumonia; gram stain is negative for any organisms; resolve with abx
  • complicated - bacterial invasion into the pleural space, leading to incr. # of PMNs, decr. glucose levels, pleural fluid acidosis, and elevated LDH; (ie if there is pus, (+) gram stain of pleural fluid, or pH <7.0); resolves with drainage via chest tube
  • empyema - accumulation of pus in pleural space; resolves with abx + drainage
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25
Q

rapid association: pleural fluid has a pH of 7.3

management?

A

empyema

diagnose with CT; removal of fluid by thoracostomy

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26
Q

rapid association: pleural fluid has a glucose of 59

management?

A

empyema

(anything <60 is indicative of empyema)

diagnose with CT; removal of fluid by thoracostomy

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27
Q

indications for tube thoracostomy

A

pH < 7.2

glucose < 60

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28
Q

T/F digital clubbing is a feature of COPD

A

False - it is not a feature of COPD, but is actually suggestive of another etiology (lung Ca, cystic fibrosis)

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29
Q

What is ARDs?

A

acute hypoxemic respiratory failure characterized by diffuse alveolar damage with pulmonary edema that is not due to heart failure or volume overload

patients develop severe respiratory distress and severe hypoxemia, where the ratio of arterial O2 tension (PaO2) to FiO2 is < 300

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30
Q

What is the FEV1/FVC ratio, VC, and DLCO seen in restrictive lung disease?

A

FEV1/FVC ratio = normal - increased

VC = low

DLCO = decreased

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31
Q

What is the etiology of Zenker’s diverticulum?

Where does it usually develop?

What is the standard treatment?

A

upper esophageal sphincter dysfunction + dysmotility

usually develops above the upper esophageal sphincter with posterior herniation btwn the fibers of the cricopharyngeal muscle

trmt: excision and cricopharyngeal myotomy

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32
Q

INR goal of patient with prosthetic heart valves

A

2.5 - 3.5

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33
Q

INR goal of patient with idiopathic DVT

A

2.0 - 3.0

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34
Q

4 features of nephrotic syndrome

common complication?

A

proteinuria >3-3.5 g/day

hypoalbuminemia

edema

hyperlipidemia and lipiduria

common complication: hypercoaguability with risk of venous + arterial thrombosis (commonly renal vein thrombosis, which is most common with membranous glomerulopathy)

Usually due to urinary loss of antithrombin 3, protein C/S, increased platelet aggregation, hyperfibrinogenemia due to increased hepatic synthesis, and impaired fibrinolysis

other complications: protein malnutrition, iron-resistant microcytic hypochromic anemia, increased susceptibility to infection, vitamin D deficiency

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35
Q

patient with history of asthma on inhaled albuterol, steroids, salmeterol, and cromolyn. She is admitted and given nebulized albuterol, IV steroids, and o2.

What do you expect her CBC to look like?

A

elevated WBC with leukocytosis (PMN predominance)

steroids increase the PMN count by stimulating bone marrow release and mobolizing the marginated neutrophil pool

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36
Q

∆ btwn hypertensive urgency vs emergency?

A
  • urgency - severe HTN w/o symptoms or evidence of end-organ damage
  • emergency - markedly severe HTN associated with malignant HTN or hypertensive encephalopathy
    • malignant - long-standing, uncontrolled HTN associated with retinal hemorrhages, exudates, or papilledema; can lead to malignant nephrosclerosis (ARF, hematuria, proteinuria)
    • encephalopathy - cerebral edema due to breakthrough vasodilation from failure of autoregulation, results in an insidious onset of HA, N, V followed by non-localizing neurologic sx (restlessness, confusion, seizures/coma) if untreated, can also develop SAH or ICH

severe HTN: ¨≥¨180/120 mmHg

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37
Q

Hypertensive emergency has two subtypes - what are they and what are the defining features?

A
  • emergency - markedly severe HTN associated with malignant HTN or hypertensive encephalopathy
    • malignant - associated with retinal hemorrhages, exudates, or papilledema; can lead to malignant nephrosclerosis (ARF, hematuria, proteinuria); usually seen in patients with long-standing uncontrolled HTN
    • encephalopathy - cerebral edema due to breakthrough vasodilation from failure of autoregulation, results in an insidious onset of HA, N, V followed by non-localizing neurologic sx (restlessness, confusion, seizures/coma) if untreated, can also develop SAH or ICH

severe HTN: ¨≥¨180/120 mmHg

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38
Q

Hematuria can be of two etiologies - what are they, what are common causes of each, and what does the UA normally show?

A

non-glomerular

  • gross hematuria
  • etiology: cancer, infections, PCKD, nephrolithiasis
  • UA: RBC w/o proteinuria
  • sx: dysuria, flank pain, renal colic depending on etiology

glomerular

  • microscopic hematuria (gross may be present in some)
  • etiology: glomerulonephritis or basement membrane disease
  • UA: dysmorphic RBCs, RBC casts, with proteinuria
  • sx: absent or non-specfiic (low back pain), but commonly has features of nephritic syndrome (hematuria, HTN, oliguria, elevated Cr)
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39
Q

Treatment for patients with dyspnea, orthopnea, PND, bibasilar crackles, hypoxemia

A

think: pulmonary edema, most likely due to acute decompensated heart failure (which is commonly due to LV systolic or diastolic dysfunction)
mgmt: IV furosemide + supplemental O2

40
Q

patient presents with long-standing heartburn, significant weight loss, fatigue, and smoking history

next step in management?

A

think: likely to be esophageal cancer

start with: barium swallow followed by endoscopy; if negative, proceed to CT of chest +/- contrast

41
Q

management of esophageal cancers

A

if localized: surgery +/- preop chemo/radioTx; curative

if metastatic: palliative thearpy (ie chemo/radioTx); not curative

42
Q

How to diagnose toxic megacolon?

how are these patients managed?

A

plain abdominal x-rays
dilated R or transverse colon (>6 cm), possible air-fluid levels, thick haustral markings that<br></br>do not extend across the entire lumen

≥3 of the following:

fever >38 C (100.4)

pulse >120/min

WBC >10.5

anemia

conservative mgmt: IV F, steroids, broad spectrum abx, bowel rest

subtotal colectomy with end ileostomy if colitis does not resolve

medical emergency b/c it can lead to colonic perforation

43
Q

how do patients with UC develop toxic megacolon?

A

UC patients typically have inflammation limited to the colonic mucosa, but sometimes the inflammation can extend to the smooth muscle layer, leading to muscle paralysis and colonic dilation

44
Q

CMV colitis usually affects which patient population

A

HIV+

45
Q

How do R vs L sided colon cancers tend to present?

A

both associated with ∆ bowel habits

R sided - anemia, FOBT+

L sided - bowel obstruction, constipation, abdominal pain

46
Q

25 yo M smoker recently diagnosed with UC

A

annual colonoscopy with biopsies once the disease has been present for at least 8 years (even if the disease is relatively well controlled with medications); total colectomy if dysplasia is detected

UC has an increased risk of colorectal cancers, which is proportional to the duration and extent of the disease

47
Q

rapid association: WBC casts

A

tubulointerstitial nephritis

usually drug induced (NSAIDs, diuretics, penicillin derivatives, sulfonamides, rifampin)

48
Q

most common paroxysmal tachycardia in people without structural heart disease

how is this usually managed?

A

paroxysmal supraventricular tachycardia (PSVT) - attacks begin abruptly and are characterized by HR in 160-220s; caused accessory conduction pathways that allow re-entry through the AV node

mgmt: vagal maneuvers (valsalva, carotid massage, immersion of face in cold water) increase vagal tone and decrease conduction through the AV node, which can slow the HR and often break the rhythm or adenosine

49
Q

characteristic levels of AST/ALT in patients with alcoholic hepatitis

A

AST : ALT > 2, with absolute values < 500 IU/L

50
Q

major ADR of metformin (2)

A

lactic acidosis + sepsis

51
Q

management of patient with hypernatremia

A

remember that it reflects a water deficit and usually occurs in patients who are debilitated or have altered mental status and cannot have access to free water.

mild cases: D5W 1/2NS

severe cases: 0.9% NS

52
Q

FEV1/FVC <70% with low DLCO

A

emphysema

53
Q

FEV1/FVC <70% with normal DCLO

A

chronic bronchitis

asthma

54
Q

FEV1/FVC >70 % with low DLCO

A

ILD

sarcoidosis

asbestosis

heart failure

55
Q

FEV1/FVC >70% with normal DLCO

A

musculoskeletal deformity

neuromuscular disease

56
Q

normal spirometry with low DLCO

A

anemia

PE

pulmonary HTN

57
Q

normal spirometry with increased DLCO

A

pulmonary hemorrhage

polycythemia

58
Q

How does the ABG and physical exam differ for patients with CHF vs COPD?

A

ABG

  • CHF: hypoxia, hypocapnia, respiratory alkalosis (secondary to tachypnea)
  • COPD: hypoxia, respiratory acidosis

PE

  • CHF: decreased breath sounds, bibasilar crackles, history of CAD, uncontrolled HTN,
  • COPD: widespread bilateral wheezes
59
Q

pt recently diagnosed with colon cancer presents with a sudden onset of severe dyspnea and L sided chest pain, followed by syncope. BP 86/50, P 120/min and regular. O2 sat 80% on RA, JVD 13cm

diagnosis?

what would you expect to see on further work-up of this patient?

A

PE

malignancy/pro-thrombotic state + acute onset of dyspnea, chest pain, tachycardia, hypoxia, and clear lungs = PE

patients with an acute massive PE can present initially with syncope & hypotension (due to low arterial perfusion)

TTE: RV dilation & failure due to RVOT obstruction & increased PVR

EKG: RBBB and R axis deviation

60
Q

rapid association: patient on anticoagulation presents with arterial + venous thrombsis

A

heparin induced thrombocytopenia type 2 (“two types - immune-mediated)

venous thrombosis can lead to DVTs, PE, skin necrosis

Arterial thrombosis can lead to acute limb ischemia, organ infarction (mesentery, kidney), and stroke

61
Q

64 M with type II DM, HTN, HLD, HT, and CKD presents with sharp, L sided CP for the last 24hrs that is worsened by deep breathing and relieved by leaning forward. PE shows friction rub at LLSB, EKG shows asymmetric T-wave inversion

Glu 248, Na 135, K 5.4, BUN 96, Cr 5.1

Diagnosis and management?

A

uremic pericarditis

common in patients with CKD, esp those with BUN >60 mg/dL

does not present wtih classical EKG findings of pericarditis (diffuse ST elevations)

treatment: dialysis

62
Q

type of murmur that is typically auscultated in IVDU patients

A

tricuspid regurgitation - holosystolic murmur that increases with inspiration

63
Q

first-line therapy for controlling anginal symptoms and improving exercise tolerance in stable angina pectoris

alternatives to patients with contraindications to ß blocker therapy (hypotensive, bradycardic)

A

ß blockers - reduce myocardial oxygen demand by decreasing the HR and myocardial contractility

alternatives: long-acting nitrates (isosorbide dinitrate or mononitrate) or Ca channel blockers (diltiazem, felodipine)

64
Q

pt presents with exertional SOB, pounding heart sensation esp if he lays on his left side, and a BP 150/45

A

Aortic regurgitation

“pounding heart sensation” = AR results in increased LVEDV, resulting in an enlarged LV that is closer to the chest wall, esp in the L lateral decubitus position

widened pulse pressure (150/45)

exertional dyspnea = insufficient delivery of O2 to peripheral tissues

65
Q

T/F patients suffering from acute pain s/p injury should receive the same standard of pain management regardless of addiction history

A

TRUE

ex: patient with an extensive history of opioid abuse should still get IV morphine if he is suffering an acute, severe pain

66
Q

Patient receiving blood transfusion suddenly develops wheezing and progresses to respiratory distress. He becomes hypotensive and soon loses consciousness

what type of patients is this reaction most common in?

what should you do next?

A

anaphylactic shock

common in patients with IgA deficiency due to the presence of anti-IgA IgG antibodies

stop transfusion -> administer Epi IM, vasopressors, histamine blockers, steroids, mechanical ventilation

67
Q

most common adverse reaction to blood transfusion

when and why does it occur?

A

febrile non-hemolytic transfusion reaction

occurs within 1-6 hours of transfusion

occurs because during blood storage, leukocytes release cytokines that when transfused, cause transient fevers, chills, malaise

68
Q

rapid association: boggy and erythematous nasal mucosa

how do patients typically present?

treatment?

A

non-allergic rhinitis (NAR) aka vasomotor rhinitis

nasal congestion or stuffiness, post-nasal drip (dry cough), no specific identifiable triggers

IN antihistamine + steroids

69
Q

how do you differentiate non-allergic rhinitis vs allergic rhinitis?

A

non-allergic rhinitis - nasal congestion/stuffiness, post-nasal drip (dry cough), and no identifiable triggers (typically negative serum radioallergosorbent test (RAST))

allergic rhinitis - eye symptoms, itching, sneezing, specific triggers

70
Q

patient presents with colicky flank pain with radiation to the scrotum; CT shows 4mm stones in the R upper ureter.

next step in management?

A

increase fluid intake >2 L /day - purpose is to increase the urinary flow rate an dlower the urinary solute concentration, thereby preventing stone formation

71
Q

where is brocas area located?

associated symptoms?

A

dominant frontal lobe

broken speech PLUS contralateral weakness of the face/extremities due to its proximity to the motor cortex and conjugate gaze deviation to the side of the leson

72
Q

when is an endoscopy vs PPI indicated for a patient with GERD?

A

endoscopy if there are “alarm symptoms” - dysphagia, odynophagia, weight loss, anemia, blleeding, recurrent vomiting, male >50, history of smoking

PPI if patients do not meet initial endoscopy criteria

73
Q

acute management of patients who present with cluster HA

prophylactic management?

A

100% oxygen = most rapid acting and effective in aborting the pain during an acute attack

verpamil = prophylaxis

74
Q

what is the hemi-neglect syndrome?

where is the lesion typically located?

A

patient neglects the LEFT side of a space and responds only to stimuli that comes from the RIGHT side (ie patients may shave only the right side of their face, comb the right side of their hair, etc)

lesion in RIGHT (non-dominant) parietal lobe, which is responsible for apatial organization

75
Q

patient with acne vulgaris and dysmenorrhea started taking oral contraceptives and becomes icterus. Liver biopsy shows dark granular pigment in hepatocytes

A

Dubin Johnson Syndrome - disorder of bile secretion that results in conjugated hyperbilirubinemia; liver is B-L-A-C-K!

(pigmented granules are not seen in the hepatocytes of Rotor syndrome)

76
Q

which nerve dysfunction is most likely responsible for impaired corneal sensation secondary to corneal abrasion?

A

trigeminal (V1), specifically to the nasociliary nerve mediating teh afferent limb of the corneal reflex

77
Q

patient recently diagnosed with systemic sclerosis presents with HA, increasing dyspnea, malaise, and nausea. BP 235/117, P 120, Hg is 6.9, Plt 57K, Cr 3.8

diagnosis? what is likely to be seen on the peripheral blood smear?

A

scleroderma renal crises - HTN + AKI in the setting of systemic sclerosis, usually within the first 5 years of SSC diagnosis

peripheral smear: schistocytes + thrombocytopenia

78
Q

2 diagnostic tests for Multiple Sclerosis

A

MRI +/- gadolinium

oligoclonal IgG bands on CSF analysis

79
Q

patient presents with transient monoccular vision loss, family history of stroke, and carotid bruit

A

fibromuscular dysplasia - non-inflammatory/non-atherosclerotic condition caused by abnormal cell development in the arterial wall taht can lead to vessel stenosis, aneurysm, or dissection

80
Q

fibromuscular dysplasia

what is it?

who does it usually affect?

which arteries does it normally affect and what type of symptoms present?

diagnostic test?

A

non-inflammatory/non-atherosclerotic condition caused by abnormal cell development in the arterial wall taht can lead to vessel stenosis, aneurysm, or dissection

affects women 15-50

commonly involves

renal arteries -> HTN

carotid + vertebral arteries -> HA, pulsatile tinnitis, dizziness, TIA, stroke, amaurosis fugax

diagnostic test: CT angio of the abdomen or duplex US

81
Q

after a central venous catheter is placed, what should be the next step in management?

A

get a portable CXR to confirm proper placement of the catheter tip and absence of complications* before administering drugs or other agents through the catheter

arterial puncture, pneumothorax, hemothorax, thrombosis, air embolism, sepsis, vascular perforation, myocardial perforation leading to tamponade

82
Q

inheritance pattern & clinical features of patients with hemophilia A & B

A

X-linked recessive - occurs exclusively in males

hemarthrosis

intramuscular hematoma (bleeding into skeletal muscle)

GI/GU bleeding

prolonged PTT

83
Q

best diagnostic test patient who complains of hearing loss and has multiple cafe au lait spots

A

acoustic neuroma -> MRI + gadolinium enhancement

84
Q

histological ∆ btwn Crohn’s and UC

A

Crohns: non-caseating granulomas

other features of Crohns: can affect any part of the GI tract but commonly limited to terminal ielum, transmural involvement, skipped lesions, cobblestone appearance, creeping fatty appearance of mesentary, fistulas, fissures, perinanal disease

UC: crypt abscesses

other features of UC: limited to the colon/rectum but may sometimes involve the terminal ileum (backwash ileitis); abdominal pain + bloody diarrhea

85
Q

most common cause of lower GI bleed in an elderly patient

A

diverticulosis - painless bleeding

colon cancer

ischemic colitis

brisk upper GI bleed (usually presents with hematemesis as well)

colonic AVM

coagulopathy

86
Q

∆ btwn diverticulosis and diverticulitis

A

diverticulosis - non-inflammed diverticula, painless bleeding (caused by diverticula eroding into a penetrating colonic artery, resulting in a profuse self-limited bleeding per rectum)

diverticulitis - obstruction of diverticula resulting in abd pain + infectious sx, usually w/o bleeding

87
Q

68 M with COPD, CHF, CAD presents wtih dyspnea, productive cough, fever x3 days. CXR shows lower lobe infiltrate.

diagnosis? management?

A

community acquired pneumonia

mgmt: determine if he/she can be managed as out-pt or in-pt using the CURB-65 algorithm (1 pt each, ≥2 = inpatient trmt, ≥4 = ICU admit)

Confusion

Uremia (BUN >20)

tachypnea (RR >30)

hypotension (BP <90/60)

Age >65

88
Q

common causes of CAP

treatment?

A

S. pneumoniae

Haemophilius

Atypical organisms (mycoplasma)

for heatlhy patients with CAP: doxycycline or macrolides

for patients requiring hospitalization: broad-spectrum fluoroquinolone (levofloxacin, moxifloxacin) or ß-lactam + macrolide

89
Q

common acid/base abnormality caused by PE

A

respiratory alkalosis - patient hyperventilates to overcome hypoxia and V/Q mismatching

90
Q

what is the mechanism behind heparin-induced thrombocytopenia?

A

heparin binds to platelet factor 4 (PF4), which triggers IgG antibodies to bind to it. This complex then activates platelets by binding to the platelet Fc receptor -> release of procoagulants -> platelet aggregation, thrombin formation -> arterial + venous thrombosis

Splenic macrophages removes the activated platelet-antibody-heparin-PF4 complexes -> thrombocytopenia

91
Q

what is the serum and urine osmolality in patients with SIADH?

A

low plasma osmolality (<280 mOsm/kg)

high urine osmolality (>100-150 mOsm/kg)

ADH draws water out of the collecting ducts -> thereby diluting serum but concentrating urine

92
Q

patient develops an acute onset of chest pain; EGK shows STEMI in leads II, III, aVF; PE: holosystolic murmur at the apex, bibasilar crackles

diagnosis?

A

mitral regurgitation secondary to papillary muscle displacement, which can occur acutely as in this case or 2-7 days after the infarct due to papillary muscle rupture

the papillary muscle displacement can lead to an abrupt diastolic volume overload, which causes elevated LVEDP/LV filling pressure -> this pressure is reflected back into teh L atrium and pulmonary circulation, and is responsible for the signs and symptoms of acute pulmonary edema and CHF

93
Q

40 yo alcoholic presents to the ED with confusion, gait instability, and horizontal nystagmus and conjugate gaze palsy in both eyes with absent ankle reflexes in both legs.

vitamin deficiency?

A

This triad of encephalopathy, oculomotor dysfunction, and gait ataxia is classic for Wernicke’s encephalopathy, which is the result of thiamine (B1) deficiency secondary to chronic alcoholism

DO NOT CONFUSE WITH COBALAMIN B12 DEFICIENCY, which also causes neurologic deficits, including impaired vibratory and position sense and gait abnormalities (due to DCML degeneration) and mental status changes. Oculomotor symptoms are usually <u>absent</u>

94
Q

alternatives to heparin in a patient who has developed HIT

A

direct thrombin inhibitors (argatroban, bivalirudin)

synthetic pentasaccharide (fondaparinux)

95
Q

Management of a patient with an EKG that shows a first-degree AV block (prolonged PR interval) with normal QRS duration

What if it showed a first-degree AV block with prolonged QRS duration?

A

First degree AV block with normal QRS duration- due to delayed impulse transmission from atria -> ventricles, usually at the AV node; requires no further evaluation unless there is significant bradycardic symptoms (ie syncope)

First degree AV block with prolonged QRS duration (>120 msec)- due to conduction delay below the AV node, usually in bundle branches; requires further evaluation to determine the site of conduction delay because these have an unpredictable progression to advanced 2nd-deg or complete heart block

A - Step II (2 decks)

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