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Internal Med > Firecracker 10/27 > Flashcards

Firecracker 10/27 Flashcards

1
Q

STEMI - EKG

A

hyperacute T waves
T wave inversions
ST segement elevation
Q waves

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2
Q

ST segment elevation =

A

transmural ischemia

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3
Q

Leads II, III, aVF

A

inferior

posterior descending artery or marginal branch.

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4
Q

Leads I, aVL, V4-V6

A

Lateral infarct of the left anterior descending artery or circumflex.

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5
Q

Leads V1, V2, V3

A

septal infarct of LAD

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6
Q

Leads V4, V5, V6

A

anterior infarct of LAD

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7
Q

serum cardiac enzymes for STEMI

A

cardiac-specific troponin T (cTnT),
cardiac-specific troponin I (cTnI),
creatine kinase MB-isoenzyme (CKMB)

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8
Q

troponins for STEMI

A

more specific and sensitive

elevated for 7-10 days after

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9
Q

CKMB for STEMI

A

rises within 8 hours

returns to normal after 72

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10
Q

AV block

A

impaired conduction between the sinoatrial (SA) pacemaker and the ventricles.

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11
Q

First Degree AV Block

A

PR > 0.2

normal 1:1 P:QRS ratio

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12
Q

First Degree AV Block Cause

A

increased vagal tone
AV nodal dz
electrolyte disturbance
med side effect

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13
Q

Second Degree AV Block - Mobitz Type I

A

progressive PR lengething until QRS is dropped

Group Beating

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14
Q

Group Beating

A

lumping of P-QRS-T elements leading up to the dropped QRS complex.

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15
Q

Second Degree AV Block - Mobitz Type II

A

random dropped QRS

discernible ratio of P:QRS

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16
Q

Mobitz Type I Causes

A

intranodal or HIS bundle conduction defects that result from medications (e.g., beta blockers, digoxin, calcium channel blockers),
increased vagal tone, or
right coronary artery mediated ischemia.

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17
Q

Mobitz Type II Causes

A

infranodal conduction abnormality in either the bundle of His or Purkinje fibers.

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18
Q

Mobitz Type I Treatment

A

adjusting medications or pacing if associated with symptomatic bradycardia

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19
Q

Mobitz Type II Treatment

A

always treated with a pacemaker due to the increased risk of progressing to high grade or third degree AV block.

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20
Q

Third Degree AV BLock

A

P waves separate from QRS
supra-ventricular impulses completely fail to conduct impulses to the ventricles, and ventricular depolarization is initiated by pacemaker cells distal to the block

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21
Q

Third Degree AV Block causes

A

coronary ischemia

also congenital AV block, lupus, or Lyme disease

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22
Q

Third Degree AV Block symptoms

A

hypotension, dizziness, syncope

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23
Q

Third Degree AV Block treatment

A

pacemaker

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24
Q

VF most commonly associated with

A

coronary artery dz

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25
Q

VF risk factors

A

MI, decreased left EF, electrolyte disturbance

long QT syndrome, A fib

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26
Q

most common cause of mortality following MI

A

V fib

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27
Q

Patients with VF

A

sudden LOC or comatose

symptoms of MI prior to collapse

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28
Q

VF results in

A

insufficient forward cardiac output –>

CNS ischemic injury, MI, sudden cardiac death

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29
Q

initial therapy for VF

A

defibrillation followed by 2 minutes of CPR

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30
Q

VF - after 2 rounds of defibrillation

A

epinephrine (1mg bolus, then every 3-5 minutes) should be administered followed by another shock.

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31
Q

medicines to consider with VF refractory to defibrillation

A

magnesium and amiodarone

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32
Q

asystole or pulseless electrical activity

A

immediate high-quality chest compressions.

not shockable arrhythmias

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33
Q

mildly elevated LFTs

A

chronic hepatitis
alcohol induced hepatitis
NAFLD

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34
Q

LFTs 100s or 1000s

A

acute viral hepatitis

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35
Q

LFTs 10,000

A

toxin-related hepatitis

liver ischemia

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36
Q

location of AST

A

liver, cardiac muscle, skeletal muscle

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37
Q

hepatic pattern of liver disease

A

markedly elevated AST and ALt

minimal to no elevation in alk phos

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38
Q

half life of albumin

A

20 days

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39
Q

albumin in patients with advanced liver cirrhosis

A

low

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40
Q

severe liver damage labs

A

increased PT/INR

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41
Q

PHT value

A

greater/equal to 12

increased resistance to portal blood flow

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42
Q

Prehepatic PHT

A

portal vein thrombosis

schistosomiasis

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43
Q

Intrahepatic PHT

A

cirrhosis
hep B/c
PBC

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44
Q

posthepatic PHT

A

right sided heart failure
Budd-Chiari syndrome
severe TR

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45
Q

hepatic venous pressure gradient

A

balloon catheter to monitor gradient pressure btwn portal vein and IVC

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46
Q

PHT complications

A

variceal bleedings
SBP
ascites
pleural effusion

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47
Q

PHT management

A

screening for GE varices, beta blockers, diuretics, sodium restriction

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48
Q

transjugular intrahepatic portosystemic shunt

A

shunt between portal and hepatic vein (allowing portal vein to drain properly)

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49
Q

metabolic acidosis

A

ph <7.37

decrease in HCO3- levels

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50
Q

metabolic acidosis lab values

A

low pH, high H+
very low HCO3-
low pCO2
compensation - hyperventilation

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51
Q

normal anion gap values

A

10-15

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52
Q

causes of anion gap metabolic acidosis

A

methanol, uremia, DKA, paraldehyde, INH, lactic acidosis, ethylene glycol, salicylates

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53
Q

increased osmolol gap

A

suggesitive of toxic alcohol ingestion

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54
Q

OG =

A

Osm - (2Na + glucose/18 + BUN/2.6)

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55
Q

normal OG

A

<10

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56
Q

normal anion gap metabolic acidosis (hyperchloremic metabolic acidosis)

A

GI HCO3- loss
renal acidosis
drug induced hyperkalemia with renal insuff
other

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57
Q

metabolic acidosis/ GI HCO3 loss

A

diarrhea
external pancratic or small bowel drainage
jejunal and ileal loops

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58
Q

Normal anion gap hypokalemic renal acidosis

A

Type 1 and 2 RTA

acetazolamide, topiramate, amph b

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59
Q

normal anion gap hyperkalemic renal acidosis

A

Type 4 RTA (hypoaldosteronism)

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60
Q

Drug-induced hyperkalemia with renal insufficiency leading to normal anion gap metabolic acidosis is seen in

A

potassium sparing diuretics
trimethoprim
ACEI/ARB
NSAIDs, cyclosporine

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61
Q

other causes of normal anion gap metbaolic acidosis

A 
acid loads (ammonium chloride)
expansion acidosis from rapid saline adminstration
hippurate
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62
Q

urine anion gap

A

Na(urine) + K - Cl

63
Q

negative UAG

A

high levels of NH4 excretion

suggests normal renal function

64
Q

positive UAG

A

low NH4 excretion

suggests renal tubular dysfunction

65
Q

Compensation for metabolic acidosis

A

hyperventilation

cause reduction in pco2

66
Q

expected PCO2 range with metabolic acidosis

A

Winter’s formula

1.5 (measured HCO3) + 8 +/- 2

67
Q

acute and severe metabolic acidosis treatment

A

administration of NaHCo3

68
Q

absolute iron def

A

decreased iron levels in body stores

  • poor nutriion
  • impaired absorption
  • blood loss
69
Q

Functional iron def

A

insuff availability of iron to incorporate into precursors

  • anemia of chronic dz
  • treatment with erythropoiesis-stimulating agents
70
Q

anemia of chornic dz

A

hepcidin-induced block on iron release from stores

71
Q

etiology of iron def anemia

A

menorrhagia
gi bleed (colon polyp or cancer)
meckel’s diverticulum in child

72
Q

breast milk contains low

A

iron

73
Q

iron absorbed in

A

duodenum

74
Q

stages of iron def

A

loss of iron stores -> decreased ferritin –> decreased serum iron –> increased TIBC –> decreased iron sat –> normocytic anemia – > microcytic anemia

75
Q

symptoms of iron def anemia

A

pallor, fatigue
exertional dyspnea, orthostatic hypotension
tachycardia
koilonychia (spoon nails)

76
Q

plummer-vinson syndrome

A

anemia + glossitis + esophageal webs

77
Q

ferritin

A

intracellular protein that stores iron

78
Q

transferrin

A

decreased in total iron –> upregulation of transferritin synthesis

79
Q

iron def anemia gold standard

A

bone marrow biopsy - hardly ever performed

80
Q

treatment of iron def anemia

A

trial or oral iron to menstruating women

work up

81
Q

oral iron, don’t take with

A

tea, coffee, calcium (decreased absorption)

acidity (increase absorption)

82
Q

oral iron side effects

A

n/v, constipation, black stool

83
Q

dextran

A

parenteral iron

can cause life-threatening anaphylaxis

84
Q

blood transfusion for iron anemia

A 
unstable patients (hypotensive, hypoxic)
hemoglobin of 7 for healthy patients, 10 for patients with CAD
85
Q

acute mesenteric ischemia causes

A

arterial thrombus (atherosclerosis)
venous thrombus (hypercoaguable)
arterial occlusion from emboli
hypoperfusion - blood loss, CHF

86
Q

CMI cause

A

ischemia due to long standing atherosclerotic dz or 2 or more mesenteric vessels
also, vasculitidies

87
Q

CMI - age

A

over 60

females > males

88
Q

CMI - vessels

A

celiac trunk
superior mesenteric artery
inferior mesenteric artery

89
Q

AMI symptoms

A

diffuse non localized pain
N/v
bloody diarrhea

90
Q

CMI symptoms

A

postprandial pain
weight loss
n,v,diarrhea

91
Q

AMI pe findings

A

hyperactive/absent bowel sounds
positive occult blood
tachycardia

92
Q

CMI PE findings

A

malnutrition
abdominal bruit
signs of peripheral vascular dz

93
Q

diagnosis of mesenteric ischemia

A

CT angiography

94
Q

mesenteric ischemia - plan films

A

can be used to exclude perforated viscus and free air under diaphragm

95
Q

AMI complications

A

bowel necrosis, perforation, peritonitis, sepsis, death

96
Q

CMI complications

A

acute thrombosis/embolism

prolonged hospitalization due to chronic malnutrition

97
Q

AMI treatment

A

fluid resuscitation, ng tube, IV antibodies

embolectomy + thrombolytic influsion via angiography catheter

98
Q

CMI treatment

A

open or endovascular revasc

warfarin

99
Q

CMI with bowel necrosis

A

laparotmy to remove tissue

100
Q

systolic dysfunction due to

A

decreased ventricular contraction

101
Q

diastolic dysfunction due to

A

noncompliant ventricle

102
Q

causes of systolic dysfuncton

A

ischemia/CAD

anemia, myocarditis, dilated CM, fluid overload

103
Q

causes of diastolic dysfunction

A 
HTN
increased afterload (Aortic stenosis)
restrictive processes
104
Q

LSHF symptoms

A

pulmonary congestion - DOE, orthopnea, paroxysmal noctural dyspnea

105
Q

LSHF - DOE

A

caused by interstitial fluid in lung stimulating juxtacapillary receptors

106
Q

LSHF - orthopnea

A

because of increased venous return to right side of heart, worsen pulmonary congestion

107
Q

paroxysmal nocturnal dyspnea

A

gradual reabsorption of fluid from interstitium into vascular compartment that leads to increase in venous return, worses PCongestion

108
Q

LSHF - fluid overload

A

decreased CO
activates RAAS
retention of salt, water

109
Q

hemoptysis in LSHF

A

rupture of engored bronchial veins

110
Q

brick red sputum in LSHF

A

increased pressure in alevolar capillareis –> alevolar macrophages inget RBC –> hemosiderin laden macrophages

111
Q

systolic HF ausculation

A

S3 gallop - kentucky

112
Q

diastolic HF ausculation

A

S4 gallop - tennessee

113
Q

BNP cutoff

A

400

114
Q

Chest x ray findings HF

A

Kerley B lines – thin pulmonary opacities caused by fluid in the interstitium of the lung
Enlarged cardiac silhouette
Peribronchial cuffing – excess fluid in the small airway passages of the lung causes localized patches of atelectasis.
Cephalization of the pulmonary vasculature – antigravitational redistribution of the pulmonary blood flow due in part to increased pulmonary vascular resistance and pulmonary HTN.

115
Q

LSHF acute treatment

A 
Lasix (furosemide)
morphine
nitroglycerin
oxygen
positioning
116
Q

LSHF morphine

A

decreases anxiety and preload through venodilation

117
Q

Nitroglycern in LSHF

A

titrate IV SBP no less than 80

118
Q

long term treatment of LSHF

A

beta blockers
spironolactone
ACE inhibitors

119
Q

CCB and LSHF

A

not recommended

120
Q

physical findings of atypical pneumonia

A

slower onset, insidious

no signs of consolidation

121
Q

maintaining K balance

A

excreted in distal nephron
excretion enhanced with reabsorption of Na+
secretion increased by aldosterone
GI tract absorbs 90%

122
Q

pleurisy

A

any condition that causes an irritation of the parietal pleura.

123
Q

diastolic HF - echo

A

normal/high EF
decreased EDV
increased EDP

124
Q

digoxin in HF

A

symptoms relief, reduce hospitalization

no effect on mortality

125
Q

tetanus management

A

benzos
immune globulin
metronidzale or penicllin g

126
Q

lifestyle modifications for CHF

A

exercise, sodium restriction

127
Q

Mobitz Type I pathophysiology

A

intranodal or HIS bundle conduction defects that result from medications (e.g., beta blockers, digoxin, calcium channel blockers), increased vagal tone, or right coronary artery mediated ischemi

128
Q

Mobitz Type II pathophysiology

A

infranodal conduction abnormality in either the bundle of His or Purkinje fibers.

129
Q

LS CHF x ray findings

A

cardiomegaly
kerley b lines
peribronchial cuffing
cephalization of pulm vasculature

130
Q

clinical features of pleurisy

A

sharp knife like pain worse on inspiration

after preceded by URI symptoms

131
Q

emphysema

A

lung condition highlighted by pathological enlargement of distal airways due to airway destruction.

132
Q

chronic bronchitis

A

productive cough of at least 3 months per year for 2 consecutive years.

133
Q

COPD risk factors

A

smoking!!

pulmonary irritants, alpha-1 antitrypase, asthma

134
Q

protease-antiprotease hypothesis

A

Nicotine and smoke derived free radicals cause accumulation of PMNs and macrophages in the alveoli.
Activated PMNs → release proteases which result in tissue damage.
Smoking also enhances macrophage elastase activity, which is not susceptible to cleavage by α1-antitrypsin.

135
Q

functional alpha1-antritrypsin def

A

smoking derived free radicals can disrupt the balance between proteases and anti-proteases by inactivating α1-antitrypsin → “functional” α1-antitrypsin deficiency.

136
Q

COPD patient presents with

A

combination of cough (productive or non-productive) and dyspnea of insidious onset and chronic duration.

137
Q

COPD PE findings

A

Hyperinflation or “barrel chest” (increased AP diameter)
Diminished breath sounds
Hyperresonance to percussion
Prolonged expiration with “pursed lips” breathing → sudden expiration may cause atelectasis due to rapidly decreased alveolar pressure.

138
Q

obstructive pattern COPD symtpoms

A

tachypnea, tachycardia, and cyanosis.

139
Q

wheezes

A

expiratory, obstruction

140
Q

crackles

A

inspiratory, opening of collapsed alveoli

141
Q

COPD diagnosis

A

hyperinflation with an obstructive pattern, and systemic findings of hypoxemia and hypercapnia

142
Q

COPD PFTS

A 
Decreased FEV1
Decreased FEV1/FVC ratio
Decreased VC
Decreased DLCO
Increased TLC, RV, FRC (from trapped air)
143
Q

COPD ABGs

A

Chronic respiratory acidosis, leading to chronic metabolic alkalosis → elevated PCO2 and bicarbonate.
Polycythemia may occur in response to chronic hypoxemia.

144
Q

COPD CXR

A

hyperlucent lung fields. Air trapping can lead to flattening of the diaphragm. In severe disease the heart can also become elongated and tubular shaped as a result of the increased air in the thorax.

145
Q

COPD death

A 
Respiratory acidosis and hypercapnic respiratory failure
Cor pulmonale (rare)
Massive spontaneous secondary pneumothorax
146
Q

cor pulmonale occurs as result of

A

hypoxia

147
Q

increased afterload can cause

A

RV failure

148
Q

COPD treatment goals

A

reduce obstruction by dilating the airways and reducing mucus secretion, and prevention of disease progression.

149
Q

COPD treatment

A

1) smoking cessation 2) antitussives/expectoants 3) inhaled b2 agonists 4) anticholinergics 5) inhaled corticosteroids

150
Q

antitussives

A

dextromethophran

codeine-guaifenesin

151
Q

inhaled b2 agonists

A

bronchodilators

salmeterol

152
Q

inhaled anticholinergics

A

bronchodilator
ipratropium bromide
slower onset, longer duration

153
Q

inhaled corticosteroids

A

budesonide, fluticasone

Internal Med (23 decks)

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