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ABOMS > Medical Management > Flashcards

Medical Management Flashcards

1
Q

What is the murmur of a patient with aortic stenosis

A

Crescendo-decrescendo systolic murmur

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2
Q

Murmur-Aortic regurgitation

A

Decrescendo blowing diastolic murmur

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3
Q

Murmur-mitral stenosis

A

opening snap

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4
Q

Murmur-mitral regurgitation

A

Holosystolic, blowing murmur

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5
Q

Murmur-mitral valve prolapse

A

Midsystolic click

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6
Q

Murmur-mitral valve prolapse syndrome

A

Midsystolic click

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7
Q

Systolic or Diastolic HF have an S3 murmur

A

Systolic with a dilated left ventricle

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8
Q

Systolic or Diastolic HF have an S4 murmur

A

Diastolic with left ventricle hypertrophy

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9
Q

Treatment for VTachy

A

Cardioversion

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10
Q

VTach caused by

A

Myocardial infarction, cardiomyopathy, electrolyte abnormality, blunt trauma, infections or infiltrative disease

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11
Q

AFib caused by

A

HTN
Valvular disease
CAD
HF

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12
Q

AFib diagnosed by

A

Absent P waves

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13
Q

Treatment for Afib and Aflutter in an unstable situation

A

Cardioversion

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14
Q

Treatment for paroxysmal supra ventricular tachycardia (PSVT)
(4 pts)

A

Vagal maneuvers,
adenosine,
medical management,
ablation

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15
Q

WPW Syndrome-Etilogy

A

Accessory pathway between atria and ventricles due to congenital separation during fetal development; risk of sudden cardiac deaths and tachyarrhythmias

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16
Q

Bradycardia etiology?
(7 causes-4 i’s)

A

Ischemic, infectious, infiltrative, autoimmune, conditioned heart, medication, neurologic

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17
Q

CHADS scoring table

A

C-CHF
H-HTN-BP consistently above 140/90 mHg
Age>75 yrs
D-DM
S-Prior stroke or transiet ischemic attack or thromboembolism (2 is for 2 points if yes_

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18
Q

Type I Heart Block ECG finding

A

Increased PR interval

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19
Q

Type IIa Heart Block ECG finding

A

Increased PR interval until dropped QRS

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20
Q

Type IIb Heart Block ECG finding

A

Regularly dropped QRS with constant PR interval

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21
Q

Type III Heart Block ECG finding

A

Complete dissociation of P waves and QRS complexes

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22
Q

Primary HTN

A

No identifiable cause

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23
Q

2ndary HTN
(6 causes)

A

Indetifiable cause such as:
Renal artery stenosis
diabetic nephropathy
Thyroid disease
cocaine use
pheochromocytoma
OSA

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24
Q

Diagnosis of HTN

A

at least 2 elevated BP readings on 2 different occasions
Stage 1: SBP from 140-159, DBP from 90-99
Stage 2: SBP >160, DBP >100

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25
Q

Beta Blocker used for:
Side effects:

A

MI, CAD, CHF
Bronchospasm, AV node blockade

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26
Q

ACE Inhibitor
Side Effects:

A

Diabetes, MI, proteinuria, CHF
SIDE EFFECTS: Cough, Renal Failure

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27
Q

Thiazide use
Side Effects

A

Combination therapy:
Hypokalemia

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28
Q

Difference of HTN Urgency vs Emergency

A

Urgency, BP >180/120
Emergency, BP >180/120 with evidence of end organ damage

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29
Q

Duke Criteria, definite IE

A

2 major; 1 major & 3 minor; 5 minor

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30
Q

Duke Criteria, possible IE

A

1 major & 1 minor; 3 minor

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31
Q

Duke Criteria, major criteria

A

Positive blood culture, Echo with evidence of endocardial involvement

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32
Q

Bacteria associated with IE

A

Staph Aureus-IV
Native Valve-Viridans Streptoocci, S aureus, enterocci
Prosthetic Vavle-S epidermidia, S aureus
Culture Negative-HACEK organism

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33
Q

HACEK organism

A

H-Haemophilus
A-Aggregatibacter
C-Cardiobacterium
E-Eikenella corrodens,
K-Kingella

Candida, Aspergillus

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34
Q

Minor Criteria of Dukes

A

-Predisposition to IE (IV drug use, indwelling catheter, diabetes)
-Fever
-Vascular phenomena )Janeway lesions, arterial emboli, intracranial hemorrhage, splinter hemorrhage)
-Microbiologic evidence
-Immunologic phenomena (Osler nodes, Roth spots)

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35
Q

Janeway lesions

A

Janeway lesions are irregular, nontender hemorrhagic macules located on the palms, soles, thenar and hypothenar eminences of the hands,

associated with IE

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36
Q

Splinter hemorrhages

A

Associated with IE

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37
Q

Abx treatment for native valve IE with Viridans streptococci, Aureus, enterococci

A

Vanocmycin and gentomycin

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38
Q

METs

A

Metatbolic equivalent of tasks

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39
Q

METs score

A
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40
Q

What is RV, TV, ERV, and FRC

A
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41
Q

What is FEV1, FVC, TLC

A
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42
Q

Name three types of obstructive lung disease

A

COPD,
Asthma
Cystic Fibrosis

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43
Q

Name three types of restrictive lung disease

A

Sarcoidosis,
Interstital lung disease
Collagen Disorder

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44
Q

Extraparenchymal restrictive types of pulmonary disease

A

Obesity
Scoliosis
Myasthesia Gravis
Diaphragmatic Weakness
Cervical spine injury

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45
Q

Compare FEV1, FVC, FEV1/FVC, lung volume, flow rates between obstructive and restrictive lung disease

A
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46
Q

True or False, Asthma has a prolonged expiratory phase

A

True, it does have prolonged expiratory duration with expiratory wheezing

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47
Q

Mild Intermittent Asthma Definition & Treatment

A

Def: <2 days week with PEF> 80% (PEF = peak expiratory flow)
Treatment: Bronchdilator as needed like albuterol, salmeterol

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48
Q

Mild PersistentAsthma Definition & Treatment

A

Def: >2 days week, but less than 1 time a day with PEF> 80% (PEF = peak expiratory flow)
Treatment: Low-dose inhaled steroids like Fluticasone, hydrocortisone, prednisolone

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49
Q

Moderate PersistentAsthma Definition & Treatment

A

Def: daily symptoms with PEF>60% but less than 80% (PEF = peak expiratory flow)
Treatment: Low-dose inhaled steroids like Fluticasone, hydrocortisone, prednisolone & albuterol, salmeterol (beta 2 agonist)

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50
Q

Severe PersistentAsthma Definition & Treatment

A

Continuous symptoms with PEF < 60%, add oral steroids to everything mentioned above.

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51
Q

Beta 2 agonists for asthma treatmetn

A

relaxation of bronchial muscle due to increase in cAMP formation

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52
Q

Corticosteroids role in asthma treatment

A

Suppresses inflammatory response and decreases mucosal edema like Fluticasone, hydrocortisone, prednisolone

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53
Q

What is Montelukast

A

a leukotriene modifier used for asthma treatmetn which is an antagonist that decreases bronchoconstriction

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54
Q

What is Zileuton

A

A leukotriene formation inhibitor that treats asthma

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55
Q

What is ipratropium bromide used for

A

It blocks cholinergic constriction causing bronchodilation

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56
Q

Asthma vs COPD

A

Asthma is reversible, COPD is not reversible, both are obstructive lung diseases

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57
Q

Chronic bronchitis def

A

Chronic productive cough for 3 months in 2 consecutive years…blue bloater

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58
Q

What’s a pink puffer”

A

Refers to emphysema which is enlargement of airways and wall destruction distal to bronchioles, “pursed lip breathing

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59
Q

COPD its with arterial blood gas analysis will show

A

Hypercarbia
hHypoxemia

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60
Q

What deficiency can be associated with emphysema patients?

A

Alpha 1 antitrypsin deficiency

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61
Q

FEV1 can determine severity of COPD, true or false

A

True, it is on stages based on FEV which determine treatment

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62
Q

What is ARDS?

A

Acute respiratory distress syndrome associated with bilateral lung infiltrates?

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63
Q

What causes ARDS?
(6 pts)

A

Pneumonia
Aspiration
Trauma
Acute pancreatitis
inhalation injury,
Reperfusion injury

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64
Q

ARDS is diagnosid by a ration of PaO2 to FiO2 that is less than _____?

A

200

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65
Q

PE symptoms? ( 6 pts)

A

-Dyspnea,
-hemoptysis,
-fever,
-cough,
-tachypnea,
-tachycardia

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66
Q

V/Q scan in treatment PE

A

Ventilation without perfusion suggests PE

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67
Q

What anticoagulant treats PE

A

Heparin bridge to Coumadin to maintain iNR of 2-3 for at leasts 3-6 months

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68
Q

What is the modified wells criteria

A

Something that determines the likelihood of PE and if greater than 4, someone likely has PE?

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69
Q

What are the criteria for modified wells criteria? (7 pts)

A

signs/symptoms of DVT
-PE is primary diagnosis
-HR >100 bpm
-immbilized for at least 3 days or surgery in previous 4 weeks
-previous diagnosed PE or DVT
-Malignancy with treatment
-Hemoptysis
-DVT

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70
Q

What determines acute renal failure?

A

Increase in serums creatinine >0.3 mg/dL over baseline
-Urine output less than 0.5 cc/kg/hr for more than 6-12 hrs

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71
Q

Prerenal causes of renal failure?

( 3 pts)

A

volume depletion, severe liver disease, severe CHF

Treatment: Fluids

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72
Q

REnal causes of renal failure?

(4 pts)

A

Tubular injury, acute tubular necrosis, interstitial disease, globular disorder

Remove underlying agent and treat cause

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73
Q

Postrenal causes of renal failure

(3 pts)

A

Urinary tract obstruction with a fractional excretion of sodium <1%, oliguria (little urine), anuria (no urine)

Treatment: Remove obstruciton

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74
Q

Need for emergent dialysis

AEIOU

A

A-Acidosis
E-Electrolyte abnormality
I-Ingestion
O-Overload
U-Uremia

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75
Q

Chronic renal fialure

A

Permanent loss of renal function for at least 3 months caused by

HTN
DM
renal artery stenosis,
Polycystid kidney disease

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76
Q

What predicts progression of chronic renal failure

A

Protienuria

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77
Q

Complications of CRF
(6 pts)

PHAARD

A

-Pericarditis due to fluid overload
-Hyperkalemia
-Anemia
-Acidosis
-Renal osteodystorphy due to phosphate issues
-Dialysis infections

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78
Q

T/F, leukocyte esterase and nitrites and protein in abundance are found in abnormal urine

A

True, possible urine infection

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79
Q

Glucose absent in abnormal urine?

A

False, it is present due to renal fialure

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80
Q

What is primary nephrotic syndrome?

A

direct damage to glomeruli causing massive proteinuira

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81
Q

What symptoms are associated with nephrotic disease
(4 pts)

nePHHrotIc

A

-Peripheral edema,
-hypoalbuminemia,
-hyperlipidemia,
-increased proteinuria

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82
Q

Membranous nephropathy

A

Thickneing of capillary loops with sub epithelial deposits

It is a nephrotic disease meaning damage to glomeruli

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83
Q

Goodpasture syndrome

A

Linear IgG deposition along globular basement membrane

It is a nephrotic disease meaning damage to glomeruli

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84
Q

What is focal segmental glomerulosclerosis

A

Glomerulcsclerosis causing proteinuria

It is a nephrotic disease meaning damage to glomeruli

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85
Q

What is minimal change disease

A

It is epithelial foot process loss

It is a nephrotic disease meaning damage to glomeruli

Nephrotic syndrome is a group of symptoms that include protein in the urine, low blood protein levels in the blood, high cholesterol levels, high triglyceride levels, and swelling.

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86
Q

What is secondary nerphrotic syndrome

A

Damage of glomeruli secondary to systemic disease.

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87
Q

What is a kimmelstiel-Wilson lesion

A

It is a lesion associated with nephrotic syndrome and diabetes mellitus

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88
Q

What two pathologies have positive Congo red stains?

A

Multiple Myeloma & Amyloidosis

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89
Q

What is nephritic disease?

A

It is inflammatory disorder in the glomeruli

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90
Q

Glomerulonephritis

A

RBCs in urine with or without cellular casts and proteinuria

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91
Q

What symptoms are associated with inflammatory disorder in the glomeruli (nephritic diseases)

(4 pts)

A

-HTN,
-edema,
-oliguria,
-hematuria

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92
Q

Immune complex glomerulonephritis

3 conditions and assoicated renal pathology

A

Subacute bacterial endocarditis-leads to present glomerulonephritis

Post-streptococcal-Subepithelial hums

Membranoproliferative glomerulonephritis-subendothelial deposits

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93
Q

Decreased complement levels is associated with what kind of nephritic disease?

A

Immune complex glomerulonephritis

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94
Q

What is Pauci immune glomerulonephritis

A

It is glomerulonephritis associated normal complement levels

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95
Q

IgA nephropathy?

A

IgA deposits in mesangium

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96
Q

Wegners granulomatosis pathology

A

Necrotizing crescent disease

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97
Q

Churg-Struss syndrome

A

Necrotizing crescent disease

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98
Q

Discuss differences of nephritic versus nephritic disease in terms of:

-Protein
-Urinalysis
-BP
-GFR

A

Nephritic Disease- Inflammatory of the glomeruli

Nephrotic Disease-Damage to glomeruli causing massive proteinuria

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99
Q

In evaluating pH and PaCO2, how do you tell if it s metabolic or respiratory disorder?

A

Metabolic disorders - pH and PaCO2 change in the same direction

Respiratory Disorders-pH and PaCo2 change in opporsite directions

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100
Q

Discuss the differences of metabolic acidosis, alkalosis in terms of PaCO2 and bicarbonate.

A
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101
Q

How do you determine the anion gap?

A

AG: Na- (CL+HCO2) < 12

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102
Q

If aG <12, acidosis is due to…

A

loss of bicarbonate (i.e. diarrhea)

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103
Q

If AG>12, acidosis is due to increase of

A

nonvolatile acid (lactic acidosis.

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104
Q

Metabolic acidosis etiology is best determined by th emneumonic MUDPILES

A

M-Methanol ingestion
U-Uremia
D-Diabetic Ketoacidosis
P-Paraldehyde Ingestion (antiseizur medicine)
I-Isoniazid Ingestion (drug for tB)
L-Lactic Acidosis
E-Ethylene glycol ingestion (antifreeze)
S-Saliacylate ingestion (aspirin)

Remember AG>12 in these situations

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105
Q

Symptoms of Metabolic acidosis

A

Hyperventilation (compensatory_
-Decreaed tissue perfusion
-Decreased CO
-Altered mental status
-Arrhythmias
-Hyperkalemia

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106
Q

How do you manage metabolic acidosis

A

Treatment of underlying issue.

Sodium bicarbonate

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107
Q

What is metabolic alkalosis

A

Increased blood pH with increased bicarbonate

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108
Q

What are the etiologies of Metabolic alkalosis

A

1-Extracellular fluid expansion-like adrenal disorders causing increased mineralocorticoid secretion; increased reabsorption of bicarbonate and sodium and secretion of chloride
2-Extracellular fluid contraction-Vomiting, nasogastric suction causing hydrochloric acid and bicarbonate loss, excessive use of diuretics

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109
Q

What are the signs/symptoms of metabolic alkalosis

A

Hypokalemia,
elevated bicarbonate,
elevated pH,
Hypoventilation,
arrhythmia,
decrease in cerebral blood flow

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110
Q

Metabolic alkalosis, treated with?

A

Volume and K replacement

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111
Q

REspiratory acidosis diagnosis

A

Decreased blood pH with arterial PaCO2 > 40

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112
Q

What causes respiratory acidosis?

A

-COPD
-Brainstem injury
-Respiratory muscle fatigue
-Drug overdose causing hypoventilation

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113
Q

What are signs of respiratory acidosis?

A

Confusion
headaches
Fatigue
CNS

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114
Q

How to treat respiratory acidosis

A

Consider mechanical ventilation with severe acidosis, deteriorating mental status, and impending respiratory failure.

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115
Q

What is respiratory alkalosis

A

Alveolar hyperventilations with increased blood pH and a decrease in PaCO2 ( breathing quickly into a bag to help it)

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116
Q

What are the causes of respiratory alkalosis

A

-Anxiety
-Sepsis
-Pregnancy
-Liver Disease
-Pulmonary embolism
-Asthma

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117
Q

What are the symptoms of respiratory alkalosis?

A

-Decreased cerebral blood flow
-Lightheadedness
-Anxiety
-Perioral Numbness
-Arrhythmias

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118
Q

How to treat respiratory alkalosis

A

Breathe into paper bag, rebreathe CO2 and decrease the pH

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119
Q

What are symptoms of hyponatermia

A

Lethargy, seizures, nausea/vomiting, confusion

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120
Q

Hyponatremia can be caused by SIADH which stands for?

A

Syndrome of inappropriate antidiuretic hormone secreiton

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121
Q

What happens if you rapidly improve sodium levels?

A

It can lead to demyelinating encephalopathy

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122
Q

Treatment of hyponatremia

A

Depends what kind of volume status and neurologic symptoms are present.

-You can calculate the sodium deficit
-Hypovolemia-Isotonic saline
-Euvolemia-Diuresis, and infusion of hypotonic saline in symptomatic patients,
-Hypervolemia-Diuretics with addition of hypertonic saline only in symptomatic patients.

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123
Q

What are symptoms of hypernatermia

A

-Lethargy
-Weakness
-Irritability
-Seizure
-Polyuria

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124
Q

Treatment of hypernatermia

A

-Treat diabetes insepitius, replace isotonic fluid

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125
Q

Hypokalemia? better or worse than hyperkalemia

A

Hypokelimia is better tolerated than hyperkalemia

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126
Q

Symptoms of hypokalemia

A

-Muscle weakness but usually less than 2.5
-Abnormal ECT
-Prominent U waves and QT prolongation

127
Q

How to treat hypokalemia

A

Potassium replacement and magnesium replacement

128
Q

Symptoms of Hyperkalemia

A

-Poorly tolerated, especially when level is above 5.5, a patient with chronic renal disease may normally have an elevated potassium level

129
Q

Symptoms of Hyperkalemia

A

-ECG changes
-Peaked T waves, and PR interval lengthening, disappearance of p waves and QRS prolongation, final-ventricular asystole
-Respiratory failure
-Nausea/vomiting
-Muscle weakness

130
Q

How to treat hyperkalemia

A

Shift potassium intracellular with insulin and desctorse
-Diuretics
-ECG changes.

131
Q

Which has bloody diarrhea…chron’s or ulcerative colitis?

A

Ulcerative colitis

132
Q

Which has patchy transmural inflammation….Chron’s or ulcerative colitis?

A

Chron’s disease

133
Q

Which has continuous mucosal inflammation….Chron’s or ulcerative colitis?

A

Ulcerative colitis

134
Q

Which is associated with uveitis, erythema nodosum and ankylosing spondylitis…chron’s or ulcerative colitis

A

Ulcerative colitis

135
Q

Where does ulcerative colitis occur?

A

colon to th erectum

136
Q

Where does Chron’ disease occur?

A

anywhere in the GI but propensity to the illeum

137
Q

Ulcerative colitis…increased malignancy risk or decrease

A

Increased

138
Q

Diagnosis, Transmission and Treatment of Hep A/B/C

A
139
Q

Hepatitis B serology

A
140
Q

T/F: GERD is associated with adenocarcinoma and Barrett esophagus

A

True

141
Q

ESLD: Etiology

A

Chronic hepatocellular injury leads to fibrosis of liver

142
Q

Symptoms of ESLD:

A

Fatigue,
anorexia,
impotence,
mElena,
spider nevi,
gynecomastia,
jaundice,
testicular atrophy,
coarse hand tremor,
caput Medusa,
spider telangiectasia,

143
Q

Complications of ESLD

A

-Esophageal varices
-Ascites
_increase in bleeding risk
-Portal HTN
-Hepatic encephalopahty

144
Q

Child-Turcotte Pugh score

A

-Associated with ESLD and the following factors
-Ascites
-Encephalopahty
-Albumin
-Prothrombin Time
-Bilirubin

145
Q

Which type of anemia is associated with iron deficiency?

A

Microcytic

146
Q

Which type of anemia is associated with renal deficiency?

A

Normocytic

147
Q

Which type of anemia is associated withB12/Folate deficiency?

A

Macrocytic

148
Q

What symptoms are associated with microcytic, normocytic, and microcytic anemias

A
149
Q

Sickle Cell disease is caused by what

A

A homozygous defect in gene for beta-globulin that produces hemoglobin S

150
Q

What diagnoses sickle cell disease

A

Target cells, sickle cells, Howell Jolly bodies, Hemoglobin S on smear

151
Q

How do you treat sickle cell disease?

A

Folate
Hydroxyurea
Agressive Hydration
Analgesia
Oxygen
Transfuse for major surgery 9-10 g hemoglobin

152
Q

What acute complications are associated with sickle cell disease?

A

Stroke
Splenic infarc
Osteomyelitis

153
Q

FActor 8 deficiency symptoms and treatment?

A

Spontaneous bleeding, treat with desmopressin or factor replacement

154
Q

FActor 9 deficiency symptoms and treatmetn?

A

Spontaneous bleeding, prolonged PTT, treat with factor replacement

155
Q

vWF deficiency (von Willebrand disease) symptoms and treatments?

A

Symptoms: Petechiae, mucosal bleeding, epistaxis, factor 8 activity with vwF deficiency

Treatment: Desmopressin, aminocaproic acid and factor 8 replacement

156
Q

What is immune thrombocytopenia purpura

A

Normal spleen with petechiae and mucosal bleeding due to immune destruction of platelets

Treat with platelet transfusion if platelet drop below 25,000-30,000

157
Q

DIC

A

Disseminated Intravascular Coagulation-A coagulopahty associated with serious illness

158
Q

What is thrombocytopenia?

A

aThrombocytopenia is a condition that occurs when the platelet count in your blood is too low.

159
Q

What is desmopressin?

A

Desmopressin is used to treat central cranial diabetes insipidus. It is a clotting promoter and diuretic

160
Q

DIC leads to symptoms of

A

thrombocytopenia and excessing bleeding or clotting

161
Q

Diagnosis of DIC is discovered with

A

Decreased fibrinogen, platelets, increased PT/partial thromboplastin time (PTT), d-dimertest, schistocytes present

162
Q

Treatment of DIC:

A

treat underlying cause; platelets and cryprecipaite for bleeding, low-dose heparin for clotting

163
Q

What is the INR goal for patients with mechanical heart valves

A

3 to 4

164
Q

Factor V Leiden (Venous or Arterial thrombosis?

A

Venous

165
Q

Protein C/S deficiency and Heparin-INdcued Thrombocytopenia…arterial or venous thrombosis?

A

Arterial and Venous

166
Q

Lab and REversiblity for warfarin

A

INR and FFP and Vitamin K reverse it

167
Q

Heparin-Lab and REversiblity

A

Lab-PTT and platelet count
Reversability-Protamine

168
Q

Low molecular weigh heparin-Lab and REversiblity

A

Lab-Antifacotr Xa
Reversibility-No

169
Q

Fondaparinum Lab and REversiblity

A

Lab-None
Reversibility: No

170
Q

Diabigatran Lab and REversiblity

A

Lab-None
Reversability-None

171
Q

Diabetes Mellitus Daignosis

A
172
Q

Complications of DM Type I versus DM Type II

A

Complications: Diabetic Ketoacidosis for Type I DM

Complications of Type II DM: Hyperosmolar nonketontic coma

173
Q

Name complications of diabetes (7)

A

-Retinopathy
-Neuropathy
-Nephropathy
-Infections
-MI
-CVD
-Stroke

174
Q

Is glargine long acting or short acting insulin?

A

It is long acting (24 hrs

175
Q

Is lispro long acting or short acting insulin?

A

It is short acting (3-4 hrs)

176
Q

What is the mechanism of metformin?

A

It decreases insulin resistance and glucose production?

177
Q

What is the mechanism of sulfonylurea?

A

It is known as glburide and stimulates insulin release

178
Q

What is the mechanisms of meglitinide (repaglindide)

A

Stimulates pancreas to release insulin

179
Q

What is the mechanism of pioglitazone

A

Decreases insulin resistance peripherally

180
Q

What is the goal of treatment for Diabetes

A

BP < 130/85
LDL- , 100, total glycerides <150, HDL >40
Smoking cessation
HbA1c < 7

181
Q

What is good control for DM

A

HbA1c between 7-8.5 is good
Fasting glucose <130
Peak postpranidal glucose <180

182
Q

What is diabetic ketoacidosis

A

It is an insulin deficiency and glucagon excess that causes severe hyperglycemia and ketogenesis. Severe hyperglycemia causes an osmotic diuresis leading to dehydration and volume depletion.

183
Q

What are symptoms of DKA

A

-Abdominal pain
Nausea
Vomiting
Kussmaul respirations
Ketone breath
Anion gap metabolic acidosis
Marked dehydration
Tachycardia
Polydipsia
Polyuria
Weakness
Altered Consciousness

184
Q

What is a diagnosis of DKA?

A

Serum glucose >250, metabolic acidosis pH >7.3 and serum bicarbonate < 15, increased anion gap, ketonuria, ketonemia, hyperkalemia, and hyponatremia

185
Q

What is the treatment of DKA

A

IV insuline at 0.1 units/kg
-drip at 0.1 units/kg/hr
-Normal saline replacement
-Decrease insulin once AG has closed and acidosis has resolved
-Monitor K
Add dextrose to IV lfuids when glucose is below 250
-Monitor Na, K, and Mg levels

186
Q

Hypohtyroid diagnosis

A

Elevated TSH and decreased T4

187
Q

What are the symptoms of hypothyroidism?

A

fatigue,
-weight gain
-cold intolerance
-depression

188
Q

What are the symptoms of hyperthyroidism

A

-Palpitations
-Heat intolerance
-Sweating
-Anxiety

189
Q

Graves disease hyper or hypothyroidism?

A

It is hyperthyroidism and comes iwht a toxic nodule and goiter

A fib and thyroid storm are associated with hyperthyroidism

190
Q

Explain Adrenal Disorders

A

Symptoms of Weakness, postural hypotension, salt craving

Labs of Low NA, increased K, volume depletion, low glucose, elevated Ca, AM cortisol

Adrenal insufficiency

Check ACTH
-Low ACTH-2ndary insufficiency due to steroids or pituitary tumors, treatment: glucocorticoid replacement

High ACTH: Primary insufficiency due to malignancy, infections, drugs or autoimmune disease

Treatment: Minearlcorticoid and glucocorticoid.

191
Q

What is an adrenal crisis?

A

Shock, nausea, vomiting, confusion, fever,, can be fatal

192
Q

What is Addison’s disease?

A

Primary renal insufficiency.
-Etiology: Autoimmune adrenalitis, malignancy, infection.

-Symptoms: Hyperpigmenation of the oral mucosa, dehydration, hypotension, fatigue, anorexia, nausea, vomiting, diarrhea, abdominal pain, salt craving, hyponatremia, hyperkalemia

Treatment: mineralocorticoid and glucocorticoids

193
Q

What is cushing’s syndrome?

A

It is caused by exogenous steroids, pituitary adenoma, ectopic ACTH, adrenal hyperplasia.

194
Q

Symptoms of Cushing’s syndrome

A

-Moon facies
-Buffalo hump,
HTN
-Truncal obesity
-Depression
Striae
-Diabetes
-Osteopenia
-Hypokalemia
-Metabolic acidosis

195
Q

When do you have to conduct a dexamethasone suppression test or 24 hr urine free cortisol level?

A

For Cushing syndrome

196
Q

How many hormones released by pituitary gland? (6)

A

-ACTH
TSH
-LH/FSH
-GH
-Prolactin

197
Q
  1. A 22 y/o patient is s/p MVA. C/C pain right shoulder, SOB, and positive Hamman’s sign. What is the diagnosis?
A

“mediastinal crunch” produced by the heart beating against air-filled tissues. Associated with pneumomediastinum

198
Q
  1. Which NIDDM med gives rise to lactic acidosis
A

Metformin. It can also cause the GI tract to become upset.

199
Q
  1. Blood Brain Barrier – what determines what enters?
A

a. Freely crosses: high lipid solubility and CO2, non ionized

200
Q
  1. Beta-2 transferrin is what?
A

a. Beta-2-transferrin is a carbohydrate free glycoprotein produced by neuraminidase activity in the brain which is uniquely found in the cerebrospinal fluid (CSF) and perilymph.

201
Q

. Vancomycin (Red Man Syndrome). The cause of this is what?

A

28
a. Histamine release

Red man syndrome is an infusion-related reaction peculiar to vancomycin. It typically consists of pruritus, an erythematous rash that involves the face, neck, and upper torso. Intravenous dose of vancomycin should be administered over at least a 60 min interval to minimize the infusion-related adverse effects Discontinuation of the vancomycin infusion and administration of diphenhydramine can abort most of the reactions. Slow intravenous administration of vancomycin should minimize the risk of infusion-related adverse effects.

202
Q
  1. Pansystolic murmur is what type of murmur?
A

a. TR, MR, VSD - Pansystolic (Holosystolic) murmurs often occur with regurgitant flow across the atrioventricular valves

203
Q
  1. A patient on 5 Fluorouracil for beast cancer. What should the doctor be worried about?
A

a. Drug has myelosuppressive effects which can increase rise of infection and bleeding tendency by causing low WBC and platelets counts

204
Q
  1. Patient with leukemia. Why is there so much bleeding?
A

a. Decreased amount of megakaroctes which is the progenitor cell for platelets

205
Q
  1. What medications do you give to treat PSVT?
A

a. Adenosine – first line choice ACLS

206
Q
  1. What changes in respiratory function are found in the pregnant patient?
A

Minute ventilation increased 50%
Alveolar ventilation increased 70%
Tidal Volume increased 50%
Oxygen consumption increased 20%
Respiratory rate increased 15 %
Dead space no change
Vital capacity no change
Lung compliance no change
Closing volume no change or decreased
Total compliance decreased 30%
Airway Resistance decreased 36%
Expiratory Reserve vol. decreased 20%
Total lung capacity decreased 0-5%
Functional residual capacity decreased 20%

207
Q
  1. Albuterol given to a patient and an improvement in FEV1 is noted. What type of disease does this patient have?
A

a. Reversible obstructivelug disease

208
Q
  1. What labs are associated with a patient diagnoses with Paget’s disease?
A

a. Normal Ca2+, normal PO4, and elevated alkaline phosphatase

209
Q
  1. Bleeding time is increased, PTT increased. What coaguloathy is present?
A

a. von Willdebrands

210
Q
  1. Removal of the parathyroid glands leads to what lab changes?
A

a. Ca2+ down and PO4 up

211
Q
  1. What are the signs of a massive P.E.?
A
  • Massive P.E. – syncope, cardiovascular collapse
  • Signs/ Symptoms: Tachycardia (most common sign), SOB, tachypnea, hypotension, chest pain, fever, tender lower extremity, loud pulmonary component of S2, hempoptosis with pulmonary infarct
  • Virchow’s triade: endothelial cell trauma, stasis and hypercoagulable state
  • EKG changes: S wave in I, Q in III, inverted T III
  • Homan’s Sign: calf pain with dorsiflexion of foot
212
Q
  1. A patient with ESRD preparing for anesthesia, which labs to check?
A

a. Potassium – hyperkalemia leading to cardiac issues

213
Q
  1. EKG strip after starting an IV – rhythm appeared to be regular and roughly 100 beats per minute – next step
A

a. Titrate midazolam to effect - (Patient anxious getting IV with basic tachycardia and no arrhythmia on EKG)

214
Q

What symptoms show up in hypopituitarism?

A

Depends on hormone deficiency, GH, LH/FSH, TSH, ACTH, antidiuretic hormone

215
Q

What is the etiology of hyperpitutarism?

A

Adenoma, prolactinoma

216
Q

Symptoms of hyperpituitarism?

A

Headache, vision changes, additional symptoms specific released from pituitary gland

217
Q

Hypercalcemia Symptoms

A

Moans (stupor, depression, psychosis)
Groans (nausea, vomting, constipation)
Stones (Kidney stones, nephrogenic diabetes insipidus)
Bones (arthritis fractures

Other symptoms include Weakness, hypertonia, bradycardia.

218
Q

Etiology of hypercalcemia,

A

Malignancy (parathyroid hormone-related protein)
Local osteolysis
Granulomatous disorders
Paget disease

219
Q

Treatment of hypercalcemia

A

Saline infusion for urinary excretion.
-Consider diuretics to inhibit calcium reabsorption and bisophosphonates or calcitonin when hypercalceimia is secondary to malignancy
-Glucocorticoids may be used to treat hypercalcemia in patients with multiple myeloma

220
Q

Hypocalcemia Symptoms

A

-Neuromuscular excitability (seizures, tetany)
-Chvostek sign (ipsilateral twitching of the facial muscles occurs)
-Trousseau sign (when a carpopedal spasm of the hand and wrist occurs )
-Prolonged QT interval

221
Q

Sarcoidosis and what does a lip biopsy show

A

Autoimmune disease causing noncaseating granulomas

Lip Biopsy shows minor salivary glands with noncaseating granulomas with normal-appearing mucosal tissue

Treatment: systemic steroids

222
Q

Rheumatoid Arthritis Diagnosis

A

Increased erythrocyte sedimentation rate and C-reactive protein,

Can be associated with serositis, ocular disease, amyloidosis, atherosclerosis.

223
Q

Rheumatoid arthritis includes 6 diagnoses from either…

A

Joint involvement, serology, acute phase reactants (CRP and ESR), with a duration greater than 6 weeks.

224
Q

In which classification of arthritis does movement improve pain?

A

Rheumatoid arthritis

225
Q

Differences between rheumatoid arthritis and osteoarthritis

A
226
Q

Diagnosis of Lupus and symptoms

A

Symptoms: Arthralgias, malar rash (photosensitive), oral ulcers, pancytopenia, serositis
Diagnosis: Anti-double standard DNA (anti-dsDNA), antinuclear antibody (ANA testing, anti-Smith antibodies, antiphospholipid antibodies.

227
Q

Myasthenia Gravis Definition

A

Autoimmune disorder with auto-antibodies to acetylcholine receptor

228
Q

Treatment of Myasthenia Gravis

A

Physostigmine (anti cholinesterase inhibitor)

229
Q

Scleroderma definition and symptoms

A

Collagen overproduction
Associated with GERD, Raynaud’s disease and skin tightening.

230
Q

Progressive systemic Sclerosis

A

Disorder of connective tissue with thickening of dermal collagen bundles and fibrosis and vascular abnormalities in internal organs with symptoms of vasomotor disturbance (HTN), fibrosis, skin atrophy, muscle atrophy, internal organ dysfunction

231
Q

Sjrogren Syndrome Definition

A

Systemic autoimmune disease in which immune system attacks exocrine glands

232
Q

Sjrogren’s Syndrome Diagnosis

A

ANA, RF, anti-SSA/B autoantibodies
Lip Biopsy
Eye exam, Schrimer test
Sialography

233
Q

Allergies…IgE

A

Type I, anaphylaxis

234
Q

Allergies Type 2

A

Antibodiy mediated cytotoxic reactions, penicillin-induced hemolytic anemia,

235
Q

Type 4 Allergies

A

Delayed hypersensitivity activating T cells-poison ivy dermatitis

236
Q

Wegener Granulomatosis

Symptoms
Diagnosis
Pathology
Treatment

A
237
Q

Churg-Strauss Angiitis

Symptoms
Diagnosis
Pathology
Treatment

A
238
Q

Microscopic Polyangiitis

Symptoms
Diagnosis
Pathology
Treatment

A
239
Q

Giant Cell Arteritis

Symptoms
Diagnosis
Pathology
Treatment

A
240
Q

Takayasu Arteritis

Symptoms
Diagnosis
Pathology
Treatment

A
241
Q

Polyarteritis Nodosa

Symptoms
Diagnosis
Pathology
Treatment

A
242
Q

Bechet’s Disease

Symptoms
Diagnosis
Pathology
Treatment

A
243
Q

Which serology test is associated with Wegner granulmatosis?

A

ANCA

244
Q

Which serology test is associated with just lupus and sjrogren syndrome

A

Anti SSA, Anti SSB

245
Q

Cardiogenic
Neurogenic
Vasovagal
Orthostatic

Causes of Syncope

A
246
Q

Static Epilepitus

A

Continous seizure activity > 30 min or recurrent seizures without rturn of consciousness
-Treatment: Check airway, breathing, circulation, consider thiamine, glucose, bentos, phenytoin

247
Q

Seizure

A

abnormal discharge of cortical neurons

248
Q

CVA

A

Acute onset focal neurologic changes secondary to blood flow disruption to the brain.

249
Q

Ischemic Stroke

A

Emboli from internal carotid artery or heart causing blood vessel blockage

250
Q

Ischemic stroke-contrast or no contrast for scan

A

No contrast

251
Q

Hemorrhagic Stroke

A

Associated with headache and loss of consciousness with HTN being primary cause

252
Q

Intracranial bleeding-Epidural Hematoma

Vessels
Symptoms
Diagnosis
Treatment

A
253
Q

Intracranial bleeding-Subdural Hematoma

Vessels
Symptoms
Diagnosis
Treatment

A
254
Q

Intracranial bleeding-Subarachnoid Hematoma

Vessels
Symptoms
Diagnosis
Treatment

A
255
Q

Neurolepic Malignant Syndrome

A

Etiology: Decreased levels of dopamine activity secondary to dopamine receptor blockade.

Symptoms: Increased body temp, altered consciousness, diaphroesis, rigid muscles, autonomic imbalance.

256
Q

What drug is used for muscle ridigidty in Neuroleptic Malignant Syndrome?

A

Dantrolene

257
Q

Serotonin Syndrome

A

Excess of serotonergic active in the CNS and peripheral serotonin recpetroms from therapeutic drug use, recreational drug use, or drug interactions.

258
Q

Symptoms of Serotonin Syndrome ( 13)

A

-Headache
-Agitation
-Confusion
-Shivering
-Sweating
-Hyperthermia
-HTN
-Tachycardia
-Nausea
-Vomiting
-Hyper-reflexia
-Tremors
-Muscle Twitching

259
Q

Differences between Serotonin Syndrome & Neuroleptic Malignant Syndrome

A
260
Q

Is alcohol a stimulant or depressant?

A

Depressant

261
Q

What does alcohol do?

A

Enhances gamma-aminobutyric acid inhibitory tone and inhibits excitatory amino acid activity.

Abrupt removal of alcohol results in overactivty o fth eCNS

262
Q

When does delirium tremens occur?

A

Usually 36 hrs after the last drink

263
Q

Delirium tremens occurs with what symptoms

A

HTN
Tachycardia
Agitation
Hyperthemia

264
Q

Symptoms monitored for alcohol withdrawl

A

Nausea/vomiting
-Anxiety
-Visual distrubance
-Paroxysmal Sweats
-Tactile disturbance
-Orientation
-Auditory disturbance
-Headache
-Agitation
-Tremors

265
Q

Treatment for alcohol withdrawl/dilirum tremns

A

-Hydrations
-Correct eletrolyte imbalance
-Thiamine, 100 mg IV daily for 3 days, then orally daily
-Folic acid
-Benzodiazepines (long acting benzos are preferred)-clonazepam

266
Q

Parkin’s Disease: Symptoms & Treatment

A

-Resting tremor, bradykinesia, cogwheel rigidity, postural instability, symptoms begin asymmetrically

Treatment: Anticholinergics, levodopa/carbidopa, doapmine agonists, anticholinergics

267
Q

Huntington Disease

A

Progressive autosomal dominant disease (cytosine-adenine guanine expansion in DNA)

268
Q

Pathology of Huntington Disease

A

Atrophy of the caudate nucleus with symptoms of chorea, dementia, psychiatric symptoms

269
Q

Alzeheimer’s Disease

A

Unkown etiology; however theory of low acetylcholine being involved

270
Q

Alzheimer Disease Symptoms:

A

Mild forgetfulness with poor concentration and changes in personality that worsen in later stages to paranoid delusions, hallucinations and need for assitance

271
Q

Alzheimer’s Disease

A

Avoid anticholinergics, donepezil is first line agent.

272
Q

Lewy body dementia

A

Loss of cholinergic neurons and death of dopaminergic neurons

273
Q

Symptoms of Lewy body dementia

A

Variation in cognition and attention; recurrent hallucinations and Parkinson-like motor symptoms

274
Q

Treatment for Lewy body Dementia

A

Donepezil for cognition and levodopa for motor symptoms; otherwise palliation

275
Q

Shock

A

Pathophysiologic state associated with decreased tissue perfusion and hypoxia.

276
Q

Categories of Shock
Cardiogenic, Hypovolemic, Distributive

A
277
Q

Stages of Shock-Initial

A

No signs of shock but cells starting to use anaerogic metabolism

278
Q

Stages of shock-Compensatory

A

Reversible-Yes
Compensatory mechanisms try to reverse the symptoms of shock (eg hyperventilation to correct acidosis)

279
Q

Stages of Shock-Progressive

A

Rerversible-No
Compensatory mechanisms cannot correct shock symptoms, leading to worsening acidosis and decreased organ perfusion

280
Q

Stages of Shock-Refractory

A

Reversible-No
Organ failure and death

281
Q

Treatment for shock

A

Agressive IV fluid (2 Liters), except for cardiogenic shock

282
Q

Shock - Class I

A

Blood Loss < 15%, Pulse - Normal, Blood Pressure- Normal, Respiratory Rate - Normal, Urine output- Normal, Orientation- Normal
Treatment- minmal

283
Q

Shock Class II
Blood Loss
Pulse
Blood Pressure
Respiratory Rate
Urine Output
Orientation
Treatment

A
284
Q

Shock Class III
Blood Loss
Pulse
Blood Pressure
Respiratory Rate
Urine Output
Orientation
Treatment

A

Blood Loss-30-40%
Pulse-Increased, >120
Blood Pressure-Decreased
Respiratory Rate-Marked tachypnea
Urine Output-20 cc/hr
Orientation-Confused
Treatment-Agressive fluids and packed RBCs

285
Q

Shock Class IV
Blood Loss
Pulse
Blood Pressure
Respiratory Rate
Urine Output
Orientation
Treatment

A

Blood Loss->40%
Pulse-Increased, >140, non palpable
Blood Pressure-Marked Decreased
Respiratory Rate-Marked tachypnea
Urine Output-Negligible
Orientation-Comatos
Treatment-Agressive therapy

286
Q

Fever Etiology - 5 Ws

A

Wind (pneumonia)
Water (Urinary tract infection)
Walking (DVT/PE)
Wound (surgical site infection)
Wonder drugs (drug fever)

287
Q

When to give fluids?

A

Fever
Drains
Gastrointestinal Losses
Burns

288
Q

Crystalloid the gold standard for volume replacement?

A

Yes, it is

289
Q

Signs of postoperative fluid overload

A

-Pitting Edema
-HTN
-Lung crackles
-shortness of breath
-Increased jugular vein distention

290
Q

Atrial Fibrillation- 1st step

A

-Systemic illness,
-Pulmonary embolus
-Acute MI
-Thyroid Disease

291
Q

A fib EKG finding

A

Wavy EKG with loss of P waves

292
Q

Treatments of Afib include

A

Beta blockers
Calcium channel blocckers
Cardioversion
Anticoagulation

293
Q

Acute myocardial infarction diagnosis on an ECG

A

-ST elevations
-T wave Changes
-Q waves for acute MI diagnosis

294
Q

Chest Pain Work UP

A
295
Q

Postopeartive Respiratory Therapy for Asthma

A

-Supplemental oxygen
Short-acting beta agonist
Systemic steroids
-IV magneium sulfate

296
Q

Postoperative respiratory therapy for PE

A

-Supplemental oxygen
-Heparin therapy

297
Q

Postoperative Respiratory Therapy for Guillan-Barre syndrome

A

Supplemental oxygen
Mechanical ventilation
Plasmapheresis or IV immunoglobulin syndrome

298
Q

Pneumonia post-operative workup

A

Culture sputum
Unasyn or Zosyn

299
Q

Treatment for post-operative status epileptics

A
300
Q

Patients with long term/chronic steroid use include:

A

-People taking a daily dose of 20 mg or more of prednisone
-More than 3 weeks of steroid treatment
-An accute cortisol deficiency secondary to surgical stress with in a patient with adrenal insufficnecy

301
Q

5 conditions that require abs prophylaxis prior to procedures

A

-Prosthetic cardiac valve
-Prosthetic material for cardiac valve repair
-Hx of IE
-Congenital heart disease
-Unrepaired cyanotic CHG within 6 months of repair
-Repaired CHD with residual disease
- cardiac transplant patients who have developed valvulpathy

302
Q

Are dialysis patients, joint replacement patients, or solid organ transplant patients required to receive prophylaxis.

A

Nope, only if recommended by their doctor.

303
Q
  1. Temporal arteritis. Patient with jaw clicking, photophobia, and intense HA. Biopsy temporal artery shows arteritis. What is the best treatment?
A

a. Methylprednisolone: high doses of corticosteroids may be given at 1-2 mg/kg/d until the disease activity is suppressed adequately

304
Q
  1. 5 yo w/ URI develops buccal cellulites w/ blue hue, what is cause?
A

a. H. influenza

305
Q
  1. Why is a cranial bone graft for midface reconstruction used in place of an AICBG?
A

a. Less resorption

306
Q
  1. Cat scratch disease. What organism responsible?
A

a. Gram negative rods, Bartonella henselae

307
Q
  1. Patient with impacted supernumerary teeth and multiple osteoma?
A

a. Gardner syndrome - sebaceous cysts, osteomas, desmoids tumors, gastrointestinal polyps, multiple teeth,

308
Q
  1. Chest x ray. Pt s/p MVA, c/c SOB, hypotension and trachea deviation. CXR shows right tension pneumothorax. How would you manage?
A

a. Needle decompression

  • In a tension pneumothorax
    1. The patient is hypotensive with acute respiratory distress
    2. The trachea may be shifted away from the affected side
    3. Neck veins may be engorged
309
Q
  1. Chest x-ray with description of trauma and pulmonary findings of tachypnea, increased resonance, absence of breath sounds?
A

a. Pneumothorax

310
Q
  1. Child sustained kicked in the face and the traumatized tissue turned blue hue. What is oraganism?
A

a. H. influenza

311
Q
  1. Mechanism of action of cyclosporine?
A

a. Inhibits the production of interleukin IL-2 by helper T-cells thereby blocking T cell activation and proliferation

312
Q
  1. Tinel’s sign is due to what?
A

a. Tingling or electric sensations in a nerve upon percussion – Distal tingling to percussion

313
Q
  • Glossopharyngeal neuralgia
A
  • Glossopharyngeal neuralgia (GN) is described as sharp, jabbing, electric, or shock like pain located deep in the throat on one side. Generally located near the tonsil although the pain may extend deep into the ear. It is usually triggered by swallowing or chewing. Treatment: carbamazepine (Tegretol®) and gabapentin (Neurontin®)
314
Q
  1. How is glossopharyngeal neuralgia distinguished from trigeminal neuralgia?
A
  • Distinguished from trigeminal neuralgia based on the pain’s location or results of a specific test. Touch the back of the throat with a cotton-tipped applicator. If an attack results, apply a local anesthetic to the back of the throat and repeats the test. If the anesthetic prevents an attack, the diagnosis is glossopharyngeal neuralgia.

ABOMS (9 decks)

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