Medicine Flashcards

1
Q

Meds to use in CF

A

BDs, Abx, anti-inflammatory agents, Pulmozyme (DNAse), Creon, Vit ADEK supplements

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2
Q

Features of Silicosis

A

miner, dyspnea/dry cough, RLD, hilar LAD with eggshell calcifications

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3
Q

Tennis-racket shaped Birbeck granules

A

Eosinophilic granuloma

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4
Q

Spirometry in COPD

A
  1. Super increased TLC and increased FRC
  2. Super decreased FEV1 and decreased FVC
    Think: air trapping, hyperinflated lungs, must breathe out slowly (super dec FEV1)
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5
Q

Therapy escalation for COPD

A
  1. Quit smoking
  2. SABD: SABA or SAMA
  3. LABD: LABA or LAMA
  4. Inhaled corticosteroids
  5. O2 therapy
  6. Lung volume resection
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6
Q

What are the BDs used in COPD?

A

SABA: albuterol, metaproterenol
SAMA: ipratropium, glycopyrronium
LABA: formoterol, salmeterol
LAMA: tiotropium

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7
Q

Honeycomb lung

A

seen because of end-stage fibrotic cystic changes in the lung parenchyma, characteristic of interstitial lung diseases like IPF

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8
Q

Halitosis, hemoptysis, productive cough

A

Bronchiectasis; treat with BDs, Stx, Abx

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9
Q

What are Starling’s forces?

A

the hydrostatic and osmotic forces that determine fluid flow in and out of capillaries
(As opposed to the Frank-Starling relationship of the heart which states that SV increased with preload)

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10
Q

Pityriasis rosea

A

Self-limited rash that starts as herald patch (well-demarcated salmon colored patch) that then develops a trailing scale
*Spares the palms/soles, so if they’re involved think syphilis

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11
Q

Psoriasis

A

erythematous patch with silver scale that bleeds (excess keratinocytes 2/2 T-helper cell dysfx) on extensor surfaces, gluteal fold, and nail pitting
TX: 1st - UV light, 2nd - topical stx
**R/o lymphoma if suspicious

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12
Q

Seborrheic dermatitis

A

The rash that appears at hairlines only, looks dry and flaky - caused by Malassezia sp. so wash with selenium
*Also causes cradle cap

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13
Q

Lichen planus

A

Purple papules with white lacy top; tx w/ topical stx and UV light
*May be med-induced

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14
Q

Antibodies for each:
SLE, RA, Limited Scleroderma, Systemic Scleroderma, Drug-induced lupus, Sjogrens, AI Hepatitis/Primary Sclerosing Cholangitis, Polymyositis/Dermatomyositis, Primary Biliary Cirrhosis

A
SLE - ANA, Anti-dsDNA (nephritis)
RA - RF, CCP
LScl - anti-centromere 
SScl - anti-topo I (Scl70)
DIL - anti-histone
Sjogrens - Ro/La
AIH/PSC - smooth muscle
PM/DM - Jo
PBC - anti-mitochondrial
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15
Q

Types of lesions of keratinocytes

A
  1. Seborrheic keratosis - senile wart, “stuck on”; benign
  2. Actinic keratosis - felt not seen; pre-malignant so cryo/5-FU
  3. SCC - ulcerative; malignant so resect it
  4. Keratoacanthoma - SCC that resolves spontaneously; still gonna biopsy it
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16
Q

Ash leaf spots

A

Confirm the spots with Woods lamp test, but the dx is clearly:
Tuberous sclerosis - look for Shagreen spots (elevated fleshy plaques) and adenoma sebaceum (hyperplastic blood vessels)
*Make diagnosis at birth to prevent MR/sz

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17
Q

Ranson’s criteria

A
GALAW - for admission criteria:
G - glucose >200
A - age >55
L - LDH >350
A - AST >250
W - WBC >16

CHOBBS - for 48hr criteria:
Ca, Hct, O2, BUN, Base deficit, Sequestered fluids

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18
Q

Rome Criteria

A

sx (at least 2 of 3) are present for at least 12wks in past 12mo:

  1. pain relieved by defecation
  2. onset assoc’d with change in stool frequency
  3. onset assoc’d with change in stool form/appearance

If criteria are met, no tests to be done

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19
Q

Treatment for pertussis

A

*Abx only help the pt if started early, but will help prevent spread to others
Azithro x5d, OR erythro x14d

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20
Q

Someone comes in with N/V. How to decide differential?

A
  1. Acute onset (+/- pain after food for a while) –> pancreatitis (may be 2/2 gallstones), get amylase/lipase
  2. N/V following big meals –> gallstones, get US
  3. baby <7wks –> pyloric stenosis
  4. also with systemic sx –> viral gastroenteritis, give oral rehydration until advanced diet is tolerated
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21
Q

Centor criteria

A
  1. tonsillar exudates
  2. tender anterior cervical adenopathy
  3. fever
  4. lack of cough
    –>0-1: low chance, don’t test and don’t treat
    –>2-3: test with rapid test or culture, treat if positive
    –>4: 53% chance that test will be positive for Strep infection, may consider empiric treatment
    **NOTE: throat culture is 90-95% sensitive, rapid detection is 90-99% sensitive
    *Palatal petechiae and scarlatiniform rash are uncommon but highly specific for Strep
    Treatment is with PCN or Amoxicillin.
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22
Q

Rosacea

A

facial redness with swollen red bumps and small telangiectasias
*difference from acne = no comedo

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23
Q

Pityriasis rosea

A

a generalized, self-limited (6-12wks) papulosquamous rash; usually starts with a single herald rash, followed by bigger eruption

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24
Q

Scleritis vs Episcleritis

A

Scleritis - unilateral diffuse injection of deep scleral vessels; associated with AI disorders like RA and Wegener’s and described as a deep boring pain with associated HA & decreased vision

Episcleritis - mild irritation, not as intense pain as scleritis

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25
Q

Ottawa foot rules - should you get an Xray?

A
  1. pain at navicular or base of 5th metatarsal

2. inability to bear weight x4 steps

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26
Q

Ottawa ankle rules - should you get an Xray?

A
  1. pain in/behind malleoli

2. inability to bear weight x4 steps

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27
Q

Someone has resistant HTN. What should you suspect?

A

Primary hyperaldosteronism - can be present in up to 20% of pts with hard to control BP.
This is when there’s too much ALD produced by the adrenals. Significant fraction of these patients will not have hypokalemia, and are often women and asx. Work-up = check plasma ALD/renin ratio, if it’s >20 then prim hyperALD is likely.

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28
Q

Multiple Myeloma

A

CRAB: Calcium, Renal failure, Anemia, Bone lesions

  • there is a 1% annual risk of progression from MGUS to MM
  • for someone with MGUS, evidence of end organ damage is used to determine if it has progressed to MM
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29
Q

Polymyalgia rheumatica

A
  • stiffness in shoulders and pelvic girdle
  • check ESR; may be normal in up to 13% of pts
  • systemic sx include fever, night sweats. weight loss, malaise
  • will see dramatic response to steroids w/in 48-72hrs
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30
Q

What moves increase what murmurs?

A

Valsalva decreases venous return to the heart, thereby increases the murmur of HOCM, and makes the murmur of mitral valve prolapse longer

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31
Q

How to treat Salmonella diarrhea?

A
If mild --> No meds.
If severe (fever, systemic toxicity) --> levofloxacin (or another fluoroquinolone) OR slow infusion of ceftriaxone
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32
Q

Treatment for symptomatic MVP

A

beta blockers such as propanolol

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33
Q

MCC of interstitial nephritis (drug)

A

Antibiotics

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34
Q

How to treat a-flutter?

A

If HDS: verapamil or digoxin

If not HDS: electrical conversion

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35
Q

Best topical treatments for chronic plaque psoriasis?

A

steroids and vitamin D

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36
Q

What is intertrigo, what is cutaneous erythrasma, and what is the treatment?

A
  • intertrigo = inflammation of skin folds caused by skin-on-skin friction
  • cutaneous erythrasma = small reddish brown macules caused by bacterial infection; can present as complication of intertrigo
  • Intertrigo complicated by erythrasma is treated with TD/PO erythromycin
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37
Q

Paronychia

A

tenderness, erythema, swelling, and retraction of the proximal nail fold in people who excessively soak or wash their hands

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38
Q

Hgb goal for anemia of CKD

A

10-12

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39
Q

What are the normal intervals for PR and QRS?

A

PR: 120-200msec
QRS: 80-100msec (<120msec)

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40
Q

What is the PR interval in AV block?

A

> 120msec, or so long that a P wave is not followed by a QRS

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41
Q

Left BBB on ECG

A

QRS >120msec; no R wave in V1; V6 will have the M shape (notch)
WLM

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42
Q

Right BBB on ECG

A

QRS >120msec; RSR’ complex (rabbit ears) -
V1 will have a large terminal R wave because R side (V1) got its depolarization late
MRW

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43
Q

Long QT syndrome

A

QT >440msec; this is a congenital disorder that predisposes to ventricular tachyarrhythmias

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44
Q

How to tell R atrial vs L atrial abnormality?

A

Look at the P wave in Lead II:

  • R (pulmonale): P wave height in lead II is >2.5mm
  • L (mitrale): P wave width in lead II is >120ms; may see notched P waves in lead II as well
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45
Q

How to tell LVH from EKG

A

S in V1 plus R in V5 or V6 is really big (>35mm)

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46
Q

Kussmaul’s sign

A

increased JVP during inspiration, from something wrong with the R ventricle
- can be caused by R ventricular infarct, cardiac tamponade, tricuspid regurg, constrictive pericarditis

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47
Q

Pulsus paradoxus

A

decrease in SBP on inspiration, due to pericardial tamponade, or asthma/COPD/tension PTX

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48
Q

Pulsus parvus et tardus

A

(weak and delayed pulse)

from aortic stenosis

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49
Q

Causes of A-fib

A
PIRATES:
Pulm disease
Ischemia
RHD
Anemia/Atrial myxoma
Thyrotoxicosis
Ethanol
Sepsis
*Chronic Afib can be from HTN, CHF
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50
Q

How to recognize A flutter on EKG?

A

sawtooth waves

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51
Q

How to recognize multifocal atrial tachycardia?

A

at least 3 different P wave morphologies; do rate control (verapamil or BB) and treat underlying cause (could be 2/2 COPD, hypoxemia, etc.)

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52
Q

What rhythm do tombstones and sawtooth represent?

A
Tombstones = V-tach
Sawtooth = A-flutter
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53
Q

Treatment for torsades

A

Magnesium
Cardiovert if unstable
Correct potassium and stop offending drugs

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54
Q

Acute CHF management

A
LMNOP:
Lasix
Morphine
Nitrates
Oxygen
Position (upright)
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55
Q

What BNP is c/w CHF?

A

BNP >500

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56
Q

Medications to treat HF by class

A
I - ACEi/ARB and BB
II - Loop diuretics
III - ISDN-Hydralazine, Spironolactone
IV - Inotropes
*If EF <35% but not in class IV, give AICD
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57
Q

How to treat dilated cardiomyopathy

A
  • address the underlying issue (Alcohol, beriberi, viral myocarditis, cocaine, drugs like doxorubicin)
  • diuretics, ACEis/ARBs, BB; digoxin 2nd-line
  • ICD if EF<35%
58
Q

Causes of Dilated CM

A
AAABCCCDEG Plus:
Alcohol, Acromegaly, Azathioprine
Beriberi
Coxsackie, Chagas, Cocaine
Doxorubicin
Endocrinopathies
Genetics
Pregnancy
59
Q

Causes of Restrictive CM

A

Infiltrative diseases: amyloidosis, sarcoidosis, hemochromatosis, fibrosis 2/2 genetic syndromes or chest radiation, lysosomal storage disorders, systemic sclerosis

60
Q

Treatment of RCM

A

basically palliative, use caution with diuretics (if fluid overloaded) and vasodilators

61
Q

Treatment of HOCM

A
  1. Avoid high contractility (i.e., intense physical activity), and anything that decreases preload (VDs/diuretics)
  2. Give Beta blockers and CCBs to slow HR and decrease contractility
62
Q

How to change the murmur in HOCM and why

A

Passive leg raise = increase pre-load –> increase chamber size –> decrease magnitude of LVOT obstruction –> decrease murmur intensity

Valsalva/Standing = decrease pre-load –> smaller chamber and more closed outflow tract, louder murmur

63
Q

MONA-BASH

A
Treatment for ACS:
Morphine
Oxygen
Nitroglycerin
ASA
Beta blocker
ACEi/ARB
Statin
Heparin
**Only ASA and BB have mortality benefit
64
Q

How to diagnose STEMI vs NSTEMI

A
STEMI = EKG (ST segment elevation >0.2mV)
NSTEMI = serial cardiac enzymes + EKG (no ST segment elevation)
65
Q

Prinzmetal angina

A

angina caused by coronary vasospasm; may see STE on EKG but there will be NO enzyme elevation which is how you tell it’s not a STEMI

66
Q

How to treat NSTEMI and STEMI

A
NSTEMI = urgently to cath lab
STEMI = emergently to cath lab

If angio shows 1-2 vessels blocked –> stent; if 3+ blocked –> CABG.
If door-to-balloon time is >90min because they have to be transferred, give tPA (door to tPA time should be <60min).

67
Q

How to treat stable and unstable angina

A
Stable = r/o MI; then get elective stress test and do risk factor reduction
Unstable = give UFH, enoxaparin, or Plavix; if not improving then go to cath lab
68
Q

Things to watch with digoxin

A
  1. renal function - RF can increase digoxin concentration, leading to toxicity
  2. K status - digoxin can cause hyperkalemia; while hypokalemia will exacerbate digoxin toxicity
  3. GI AEs - including N/V/abdominal pain
  4. Xanthopsia
69
Q

Conditions for which BB are first line

A
  • during ACS or after MI
  • heart failure
  • HOCM
  • migraine ppx
  • Graves and thyrotoxicosis
  • essential tremor
  • can also treat arrhythmias
70
Q

Time frame and clinical picture for Dressler syndrome

A
  • 2-10 weeks post-MI

- fever, pericarditis, pleural effusion, leukocytosis, increased ESR

71
Q

Post-MI complications timeline

A

D 1: HF
D 2-4: arrhythmia, pericarditis
D 5-10: LV wall rupture (will find with PEA), papillary muscle rupture (will find severe MR)
Wks-Mos: ventricular aneurysm, CHF, arrhythmia, persistent ST elevation, MR, thrombus formation
*Avoid steroids following MI as these can increase risk of rupture

72
Q

Who gets a statin?

A

People with…

  • Vascular disease (CAD, sx carotid dz, PAD, AAA, DM)
  • LDL ≥190
  • If LDL is 70-189 and age 40-75, then they need an extra thing to say yes statin - like DM or high calculated risk
  • ->These people get a high-intensity statin.
73
Q

High vs. Medium Intensity Statins

A

High = Atorva 40/80 and Rosuva 20/40
Med = Atorva 10/20, Rosuva 3/10
Other meds = Simva, Prava, Lovestatin

74
Q

Causes of secondary HTN to r/o

A
CHAPS:
Cushing's syndrome
HyperALD (Conn's)
Aortic coarctation
Pheochromocytoma
Stenosis of renal arteries
75
Q

First line agents for HTN unless a containdication exists

A

Diuretics
ACEi’s
BB’s

76
Q

Tx for HTN urgency and emergency

A

Urgency: PO BB, clonidine, ACEi; lower BP over 24-48hrs
Emergency: IV labetalol, nitroprusside, nicardipine; lower BP slowly, no more than 25% over 2hrs (to prevent cerebral hypoperfusion)

77
Q

Causes of pericarditis

A
CARDIAC RIND:
Collagen vascular dz
Aortic dissection
Radiation
Drugs
Infections
Acute RF
Cardiac (MI)
Rheumatic fever
Injury
Neoplasm
Dressler syndrome
78
Q

Causes of insufficiency murmur

A

Infection

Infarction

79
Q

More venous return (squatting, leg lift) makes which murmurs louder?

A

AS, AR

MS, MR

80
Q

More venous return (squatting, leg lift) makes which murmurs worse?

A

HOCM

MVP

81
Q

Fast rhythm: Wide and Narrow QRS complexes - rhythm types and treatment?

A

Fast and Narrow: SVT (adenosine), Afib (BB/CCB)

Fast and Wide: Vtach (Amiodarone), Torsades (Mg)

82
Q

When to give atropine?

A

sinus bradycardia, 1˚ AV block, 2˚ AV blocks types I&II (be careful when giving with Mobitz type II, it can push into complete AV block)

83
Q

How does a young person get Mitral stenosis?

A

Often it’s 2/2 RHD - GAS pharyngitis can cause rheumatic fever via molecular mimicry, abs from which attack endocardium, most often the mitral valve and cause scarring, leading to mitral stenosis

84
Q

Bullous pemphigoid vs. Pemphigus vulgaris

A

BP = not as bad; bigger stable blisters with neg Nikolsky, older pts, and milder course, give prednisone

PV = BAD, this can be life-threatening; + Nikolsky, skin coming off from intraepidermal lysis; requires high dose prednisone, IVIG, MMF, rituximab

85
Q

Dermatitis herpetiformis

A

The IgA deposition in epidermis from Celiac disease; if you see this rash don’t biopsy, look for anti-TTG abs to dx Celiac, then avoid gluten
Dapsone for sx relief of rash only

86
Q

The leukemias

A
WBC >50k
ALL = kids, need ppx intrathecal chemo
CLL = geriatrics
CML-->AML = in between but CML comes first and can devolve into AML
CML = t(9;22) - Imatinib
AML = auer rods = M3, give ATRA
87
Q

Lymphomas

A
  1. Hodgkins (better prog) - Reed Sternberg cells, spreads contiguously
  2. NHL (poorer prog) - Burkitts starry sky; spreads hematogenously, treat with R-CHOP
  • Both present as NON tender LAD, +/- B symptoms –> excisional biopsy, look for cancer cells (or if neg, look for infxn)
  • *First step is to cut, then stage (these are looking for mets): CXR, CT C/A/P, then BM bx
88
Q

TTP vs ITP

A

TTP is the recognizable one - FATRN; will have low plt and schistocytes but the rest will be normal.
ITP is dx of exclusion.

89
Q

What is ARDS?

How to treat?

A

It: fluid in between the capillaries and alveoli, which collapses the alveoli and crushes the diffusion capacity of O2
Tx: to get CO2 out, keep RR up and TV low (to avoid excess pressure); to get O2 in use PEEP to keep alveoli open (not inc. FiO2!!)

90
Q

How to differentiate CHF from ARDS?

A
CHF = Inc PCWP and dec LVF
ARDS = dec PCWP and inc LVF
91
Q

HIV-related glomerular disease

A

Focal segmental glomerulonephritis

92
Q

Muscular dystrophies and inheritance patterns

A

DMD - XLR, dystrophin deletion, onset 2-3yo
BMD - XLR, dystrophin mutation, onset 5-15yo
MMD - AD, CTG repeat, onset 12-30yo

93
Q

What to do about post-nasal drip?

A

Step 1 is D/C ACEi if it’s a dry cough
Step 2 is treat with oral antihistamine (1st gen) - try this for 2-3wks
Step 3, if that doesn’t work, then do further work up or empiric treatment for GERD, cough-variant asthma, or chronic sinusitis

94
Q

When to use amiodarone in a-fib?

A

for maintenance of sinus rhythm in patients with recurrent and symptomatic episodes of A-fib
*not for someone who is asx, spontaneously converted back to sinus rhythm, or only had afib once

95
Q

Most effective action for reducing BP

A
  1. weight loss (10%)

Others: quit smoking, DASH+Na restriction (works better than Na-restriction alone but has variable results pt to pt), and exercise; none of these are as significant as weight loss

96
Q

Renal compensation for OSA-related hypoxia

A

persistent hypoxia means persistent hypercapnia; acidosis compensated in kidney by retaining bicarb at the expense of Chloride; so will see metabolic alkalosis with decreased chloride 2/2 bicarb retention

97
Q

Rheumatic fever treatment

A

IM PCN G q4wk for years or until certain age, whichever is longer:

  • no carditis: PCN x5yr or until age 21
  • with carditis: PCN x10yr or until age 21
  • with carditis and persistent valvular disease: PCNx10yr or until age 40
98
Q

Pellagra

A
  • dermatitis (rough dry scaly skin, esp. in sun-exposed), diarrhea, and dementia (or affect changes, psychosis)
  • caused by niacin deficiency (people who eat mostly only corn products)
99
Q

If someone appears to have HIV/AIDS and a PNA, assume it’s….

A

PCP - treat with TMP-SMX and also steroids which can mitigate the dip in pulmonary function that comes when the abx lyses the bacteria

100
Q

Yellow-white, fluffy, hemorrhagic lesions on the retina

A

CMV retinitis (think HIV); treat with antivirals - PO or intravital if lesions are near the fovea or optic nerve

101
Q

Medical treatment for acute thrombus of LE artery

A

Heparin

102
Q

Popliteal cyst

A
  • caused by extrusion of synovial fluid from knee joint into the gastrocnemius or semi-membranous bursa
  • it can rupture and present as knee and posterior calf pain often with an arc of ecchymosis at the medial malleolus
103
Q

Dacryocystitis

A

inflammation/infection of the lacrimal sac; usually 2/2 s. aureus or beta-hemolytic strep

104
Q

Hordeolum

A

abscess on the upper or lower eyelid

105
Q

Rapidly progressive glomerulonephritis

A
  • pt has RF w/in wks-mo
  • bx shows crescent formation
  • 3 types, diff. by IF stain:
    1. anti-GBM abs
    2. IC deposition
    3. pauci-immune
106
Q

Focal segmental glomerulonephritis

A

NEPHROTIC syndrome caused by sclerosis of a piece of the nephron with ensuing damage to podocytes and eventually decrease UOP
- common in blacks/hispanics, fat, HTN, SCD, HIV, and heroin use

107
Q

Membranous nephropathy

A

aka membranous glomerulonephritis or glomerulopathy

  • C3/IgG deposited IN GBM and stimulate GBM growth in a spike and dome shape
  • also get mesangial expansion
  • associated with solid tumor malignancies, NSAIDs, HepB, SLE, very common in adults and adolescents
108
Q

Membranoproliferative glomerulonephritis

A
  • C3/IgG deposited IN GBM and stimulate GBM growth but 3 types:
    1. deposits are subendothelial
    2. deposits are in the GBM (tram-tracks)
    3. subepithelial AND subendothelial deposits
  • associated with Hep B&C and lipodystrophy
109
Q

Minimal Change Disease

A

podocyte effacement, may get IgM in the mesangium

- MCC of nephrotic syndrome in kids and pts with Hodgkin’s lymphoma, also associated with NSAIDs

110
Q

NSAIDs and nephrotic syndromes

A

Membranous nephropathy

MCD

111
Q

Hep B and nephrotic syndromes

A

membranoproliferative glomerulonephritis

membranous nephropathy

112
Q

Obese black people with SCD and nephrotic syndrome

A

FSGS

113
Q

Rheumatoid arthritis and nephrotic syndrome

A

amyloid deposits - look for apple green birefringence.

114
Q

Presentation of PCP

A
  • fever, dry cough, dec. SaO2
  • high LDH, diffuse reticular infiltrates on CXR
  • Treat with TMP-SMX (ppx); + prednisone if low O2 sats
115
Q

MAC

A
  • fever, cough, abd pain, diarrhea, night sweats, splenomegaly
  • high Alk-phos, may have low CD4 count
  • Tx: Azithro (ppx) or clarithro
116
Q

How does hepatorenal syndrome work?

A

severe cirrhosis causes portal HTN which induces increased NO production in the splanchnic arteries, which decreases SVR and thereby BP, leading to renal hypoperfusion and worsening of kidney function

117
Q

Euthyroid sick syndrome

A

aka “Low T3 Syndrome”: pattern of thyroid hormone levels when a person is sick:
- low T3 (total and free)
- normal T4 and TSH
Just wait until after acute illness (with plenty of recovery time) to check thyroid

118
Q

Subacute thyroiditis

A

aka de Quervain: subacute because it follows an acute infection; it’s when the thyroid is inflamed and painful/tender, just as a post-viral process

  • treat sx: BB for thyroid sx, NSAIDs for pain
  • self-limited
119
Q

Hashimoto’s thyroiditis

A

chronic AI thyroiditis: diffuse goiter with prominently hypothyroid sx because the infiltration destroys the thyroid
- find anti-TPO abs, variable RAIU

120
Q

Lead poisoning - sx

A
  1. GI: abd pain, anorexia, constipation
  2. Neuro: cognitive deficits, peripheral neuropathy
  3. Heme: anemia, basophillic stippling (because Pb inhibits heme synthesis)
    * Screen with capillary lead level, confirm with venous lead level
121
Q

What do bisphosphonates do

A

inhibit osteoclast activity - they are used to stabilize bone in destructive tumors/mets (will see cancer pt with high Ca)

122
Q

Hyperosmolar hyperglycemic state

A

old person with DM2 and glucose >600, often precipitated by infection, trauma, medication, or interruption of insulin therapy

123
Q

Aortic dissection - less obvious presentation and studies

A

Can present as chest/neck pain and syncope, then you’ll see wide mediastinum on CXR and they may or may not have:

  • pericardial effusion
  • BP differential
  • hemothorax
  • stroke
  • Horner syndrome
  • abd pain or LE weakness
  • Studies for HDS pt: first - CTA, confirmation with TEE
124
Q

Low glucose in a pleural effusion means what?

A
  1. high WBCs or high bacteria - their metabolic activity is using all the glucose
  2. you’re dealing with an exudative effusion and must do further work-up
  3. Exudative effusions with gluc <60 usually 2/2: rheumatoid pleurisy, parapneumonic effusion, empyema, TB, malignant effusion, lupus pleuritis, or esophageal rupture
125
Q

Untreated hyperthyroidism can lead to

A

bone loss

126
Q

Chondrocalcinosis

A

when you can see chronic calcification of the articular cartilage on the Xray, this finding points strongly to pseudogout (CPPD crystals, rhomboids)

127
Q

Digoxin toxicity

A

typically presents as N/V, dec appetite, confusion, and weakness; +/- visual sx like scomata, yellow, blurry vision, or blindness
*renal clearance - so look for inciting dehydration, infection, AKI, etc.

128
Q

Hypertrophic osteoarthropathy (HOA)

A

digital clubbing + sudden onset thropathy (often wrists/hands)

  • subset: hypertrophic pulmonary osteoarthropathy where the HOA is associated with pulmonary disease like lung cancer, TB, bronchiectasis, or emphysema
  • smoker with HOA –> get CXR
129
Q

Neuropathic arthropathy (aka Charcot joint)

A

destructive arthritis in pts with DM and peripheral neuropathy; commonly in ankle, with obvious deformities and chronic pain

130
Q

Types of paraneoplastic syndromes

A

Lambert-Eaton
Myasthenia gravis
Dermatomyositis (Gottron’s sign - rash on dorsal fingers)

131
Q

Progression of Lyme disease

A

Early local (up to 1mo later) = erythema migrans, fatigue/malaise, mild HA, neck stiffness, myalgias, arthralgias

Early disseminated = carditis, nerve palsy, meningitis/encephalitis, conjunctivitis, migratory arthralgia, LAD

Chronic = encephalomyelitis, peripheral neuropathy, arthritis

132
Q

Dietary recommendations for kidney stones

A
  1. hydration
  2. decreased Na intake
  3. normal Ca intake
133
Q

Predominant mechanism for ventricular arrhythmias in the acute post-MI period

A

Reentry

- so someone has an MI, goes unresponsive, likely due to reentrant v-arrhythmia

134
Q

Murmur type in IVDU

A

tricuspid regurg: holosystolic murmur that increases with inspiration
*IVDU infective endocarditis MCC by s. aureus

135
Q

Preferred modality for diagnosing kidney stones

A

US, or NC spiral CT

136
Q

Diffuse ST-segment elevation on EKG - think

A

acute pericarditis, or massive MI

137
Q

Infection in a burn patient - what type and when

A

Gram positive sepsis - soon after burn

Gram negative sepsis - like 5 days after burn

138
Q

Felty syndrome

A

RA (seropositive)
splenomegaly
neutropenia

139
Q

How long can giardia last?

A

it can become chronic - you’d be stuck with diarrhea and malabsorption for a while

140
Q

How does the vagal maneuver terminate SVT?

A

by increasing PSNS activity on the AV node it can prevent AVNRT and increase AV node refractory period