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Section III (Medicine, Anesthesia, etc.) Flashcards

1
Q

Describe Acute Coronary Syndrome

A

A disease process in which major blood vessels supplying the heart are damaged/diseased by cholesterol plaques, which cause vessels to narrow. Less blood reaches the myocardium leading to acute coronary synrome

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2
Q

How does Acute Coronary Syndrome present? (symptoms of ACS)

A

Dull substernal pain, pain radiating to left arm/jaw, diaphoresis, dyspnea

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3
Q

How do you diagnose Acute Coronary Syndrome?

A

By EKG (ST segment elevation myocardial infarction vs non-ST segment elevation myocardial infarction)
Via Cardiac Enzymes

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4
Q

How do you treat STEMI, NSTEMI, unstable angina?

A

STEMI: Immediate reperfusion (angioplasty or thrombolytic therapy) within 12h of chest pain
NSTEMI: Medical therapy (ASA, b-blocker, angiotensin-converting enzyme inhibitor)
Unstable angina: Same as NSTEMI

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5
Q

What is Congestive Heart Failure?

A

Described as systolic or diastolic heart failure.
Systolic heart failure: Reduced ejection fraction (<40%), S3 murmur, dilated Left ventricle
Diastolic heart failure: Preserved ejection fraction (<50%), S4 murmur, left ventricular hypertrophy

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6
Q

What are the symptoms of CHF?

A

Chest pain, SOB, orthopnea, extremity swelling, jugular vein distention

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7
Q

How is CHF diagnosed?

A

Echo: Evaluate heart motion, ejection fraction
EKG: Evaluate changes, heart strain
Stress test: Evaluate coronary artery disease
Brain natriuretic peptide: Normal values rule out acute heart failure
CXR: Evaluate heart size, fluid in intrathoracic cavity

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8
Q

What is the classification system for CHF? How do you treat each stage?

A

Stage A-D
A: Risk of HF due to comorbidities only (tx underlining condition)
B: No symptoms but structural abnormality predisposes pt to HF (ACE inhibitor, b-blocker)
C: Structural disease with HF symptoms (ACE inhibitor, b-blocker, diuretic, salt restriction)
D: HF symptoms at rest (Medical therapy with mechanical support)

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9
Q

Describe aortic stenosis (symptoms, murmur, diagnosis, treatment)

A

-Angina, syncope, HF
-Crescendo-decrescendo systolic murmur
-Echo with severity determined by valve area and mean gradient
-Aortic valve replacement for symptomatic patients

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10
Q

Describe aortic regurgitation (symptoms, murmur, diagnosis, treatment)

A

-Progressive dyspnea on exertion, with signs of HF
-Decrescendo blowing diastolic murmur
-Echo
-Afterload reduction with systemic vasodilators and diuretics. Valve replacement in worsening cases

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11
Q

Describe mitral stenosis (symptoms, murmur, diagnosis, treatment)

A

-Gradual onset with dyspnea on exertion, right HF, pulmonary hypertension
-Ongoing snap
-Echo with severity determined by valve area and transmitral pressure gradient; a-fib often present
-Medical therapy, valvuloplasty, mitral valve replacement

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12
Q

Describe mitral regurgitation (symptoms, murmur, diagnosis, treatment)

A

-Asymptomatic increasing to dyspnea on exertion and HF
-Holosystolic, blowing murmur
-Echo
-If ejection fraction <30%, valve replacement. If EF>30%, medical therapy, but if resistant, left ventricular assist device

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13
Q

Describe mitral valve prolapse (symptoms, murmur, diagnosis, treatment)

A

-Asymptomatic
-Midsystolic click
-Echo
-None if asymptomatic

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14
Q

Describe mitral valve prolapse syndrome (symptoms, murmur, diagnosis, treatment)

A

-Chest pain, palpitations, anxiety, skin tingling, syncope
-Midsystolic click
-SVT, autonomic nervous system dysfunction
-Reassurance, lifestyle changes, stress reduction

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15
Q

Describe ventricular tachycardia (etiology, symptoms, diagnosis, treatment)

A

-Myocardial infarction, cardiomyopathy, electrolyte abnormalities, blunt trauma, infectious or infiltrative disease
-Chest pain, dyspnea, syncope
-Monomorphic uniform QRS (scar), polymorphic varied QRS (torsades)
-Cardioversion

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16
Q

Describe atrial fibrillation (etiology, symptoms, diagnosis, treatment)

A

-HTN, valvular disease, coronary artery disease, HF
-Palpitations, fatigue, dyspnea, dizziness
-Absent P wave
-Unstable: Cardioversion
-Stable: Rate control, rhythm control, use CHADS2 criteria for anticoagulation therapy

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17
Q

Describe atrial flutter (etiology, symptoms, diagnosis, treatment)

A

-Reentry circuit in the right atrium
-Asymptomatic palpitations, decreasing exercise tolerance, dyspnea
-Continuous regular atrial activity with sawtooth pattern
-Unstable: Cardioversion
-Stable: Anti-arrhythmics, consideration for ablation

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18
Q

Describe paroxysmal supraventricular tachycardia: PSVT (etiology, symptoms, diagnosis, treatment)

A

-Atrioventricular node reentry and ectopic atrial foci
-Palpitations, lightheadedness, chest discomfort
-EKG, holter monitor
-Vagal maneuvers, adenosine, medical management, ablation

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19
Q

Describe Wolff-Parkinson-White syndrome (etiology, symptoms, diagnosis, treatment)

A

-Accessory pathway between atria and ventricles due to congenital seperation during fetal development, risk of sudden cardiac death and tachyarrythmias
-Palpitations, lightheadedness, loss of consciousness
-Delta waves on ECG
-Catheter (radiofrequency) ablation

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20
Q

Describe bradycardia (etiology, symptoms, diagnosis, treatment)

A

-Ischemic, infectious, infiltrative, auto-immune, conditioned heart, medication, metabolic, neurologic
-Dizziness, weakness, fatigue, HF, loss of consciousness
-ECG, tilt table
-Unstable: ACLS
-Stable: Treat underlying cause, atropine, pacing

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21
Q

What is CHADS2?

A

Stroke risk assessment in a-fib to determine necessity of anticoagulation or antiplatelet treatment
-CHF, HTN (above 140/90 or treated w/ med), Age (>75), Diabetes, Stroke/TIA/thromboembolism (2. points).
-Score of 0 (low risk, treat w/ ASA or nothing)
-Score 1 (moderate, treat with ASA or Coumadin INR 2-3)
-Score 2 (moderate/high, coumadin to INRS 2-3)

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22
Q

What is ECG/treatment of type I heart block?

A

-Increased PR interval
-No treatment

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23
Q

What is ECG/treatment of type 2A heart block?

A

-Increasing PR interval until dropped QRS
-Pacemaker for symptomatic patients

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24
Q

What is ECG/treatment for type 2B heart block?

A

-Regularly dropped QRS with constant PR interval
-Search for cause/pacemaker

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25
What is the ECG/treatment for type 3 heart block?
-Complete dissociation of P waves and QRS complexes -Search for cause/pacemaker
26
Describe hypertension
HTN is disease process diagnosed by at least two elevated BP readings on at least two different occasions. Can be described as primary hypertension (no identifiable cause) vs secondary hypertension (renal artery stenosis, diabetic nephropathy, thyroid disease, cocaine use, pheochromocytoma, OSA -Prehypertension: 120-130/80-89 -Stage I: 140-159/90-99 -Stage II: >160/>100 -Etiology: Obesity, familial, smoking, diabetes, kidney disease -Treated with diet, weight reduction, exercise, sodium restriction, medications
27
What are common medications for treatment of HTN?
-Beta blocker (for MI, CAD risk, CHF), side effect bronchospasm, AV node blockade -ACE inhibitor (for DM, MI, proteinuria, CHF), side effect cough, renal failure -ACE inhibitor (for patients that can tolerate), side effect renal failure -Thiazide (for combo therapy), side effect hypokalemia -Calcium channel blocker (for systolic hypertension, CAD), side effect conduction blockade
28
What is hypertensive urgency and emergency and what is the treatment?
-Urgency: >180/120 with no end organ damage, tx with med therapy on outpatient basis -Emergency: >180/120 with signs of end organ damage. Admission with IV therapy
29
Describe Infective Endocarditis as well as causes.
A bacterial infection that affects the heart lining, heart valve or blood vessel. -IV drug use: Staph aureus -Native valve: Viridans strep, S aureus, enterococci -Prosthetic valve: Staph epidermidis, S aureus -Culture negative: HACEK (Haemophilus, aggregatibacter, cardiobacterium, eikenlla corrodens, kingella), candida, aspergillus
30
How is infective endocarditis diagnosed?
DUKE Criteria -Definite IE: 2 major, 1 major/3minor, or 5 minor -Possible IE: 1 major/1 minor or 3 minor Major: Positive blood culture, echo with evidence of endocardial involvement Minor: Predisposition (IV drug use, indwelling catheter, diabetes), fever, vascular phenomena, micro evidence, immunologic phemoena (osler nodes, roth spots)
31
What is the treatment for infective endocarditis?
-Native valve IE: Vancomucin and gentamicin -Prosthetic valve: Add rifampin -Treat positive cultures
32
Describe your pre-operative treatment decision algorithm for patients on cardiovascular medications.
-I would determine the urgency if surgery. -If urgent surgery with unstable/active cardiac condition, would have medical consultation and discussion with patient's cardiologist, consider surgical intervention in hospital setting. -If non-urgent surgery, would quantify procedure risk. (Dentoalveolar: low risk, Head and neck: Intermediate risk) -For low risk, would obtain medical consultation pre-operatively -For Intermediate risk: Evaluate METs -If METS above 4, consider Statin and beta blocker pre-op -If METS below 4 (unable to climb a flight of stairs, heavy housework): Statin, beta blocker, EKG, possible ACE inhibitor. Consider pre-operative testing
33
What are common types of obstructive pulmonary diseases?
Asthma, cystic fibrosis, COPD
34
What are common types of restrictive pulmonary diseases?
Sarcoidosis, interstitial lung disease, collagen disorder
35
What are common types of extraparenchymal restrictive disease?
Obesity, scoliosis, myasthenia gravis, diaphragmatic weakness, cervical spine injury
36
What are common findings in obstructive vs restrictive lung disease.
Obstructive (blue bloaters): Decreased FEV1, normal FVC, decreased FEV1/FVC, increased lung volume, deecreased flow rates Restrictive (pink, pursed lips): Decreased FEV1, decreased FVC, normal/increased FEB1/FVC, decreased lung volume, decreased flow rates. Key differences: FEV1/FVC is normal/increased in restrictive lung disease due to decreased FVC (Max volume of air that can be forcefully exhaled)
37
Describe asthma.
Asthma is a chronic obstructive reversible disorder of airway hyper-reactivity causing dyspnea, cough, wheezing and chest tightness Diagnosed by showing reversible obstructive lung disease with normal diffusing capacity. Exam with expiratory wheezing during acute exacerbations with a prolonged expiratory phase, severe attacks with pulsus paradoxus (BP decreases with inspiration), accessory muscle use, silent chest Can be classified as mild intermittent (<2 days/week with PEF >80%), mild persistent (>2 days/week but less than 1x daily PEF >80%), moderate persistent (daily symptoms with PEF 60-80%), severe persistent (continuous symptoms with PEF <60%) Mild intermittent: Bronchodilator as needed Mild persistent: Low dose inhaled steroid Moderate persistent: Inhaled steroid and long acting beta 2 agonist Severe persistent: Add oral steroids
38
Describe common medications for asthma.
-Beta 2 agonist (albuterol, salmeterol): Beta 2 agonist that relaxes bronchial muscles -Corticosteroids (fluticasone, hydrocortisone, prednisolone): Suppresses inflammatory response and decreases mucosal edema -Leukotriene modifier (montelukast): Antagonist decreases bronchoconstriction -5-lipoxygenase (zileuton): Inhibits leukotriene formation -Anticholinergic (Ipratropium bromide): Blocks cholinergic constriction causing bronchodilation
39
Describe COPD
-Nonreversible chronic airway restriction -Symptoms include: Worsening dyspnea, increases cough/sputum, hyperinflation, prolonged expiration, wheezing -Chronic bronchitis: Chronic productive cough for 3 months in 2 consecutive years (blue bloater) -Emphysema: Enlargement of airways and wall destructin distal to bronchioles (pink puffer, pursed lips) -Diagnosis: PFTs (FEV1/FVC) and postbronchodilator values (non-reversible), ABG with hypercarbia/hypoxemia, evaluate alpha-1 antitrypsin deficiency in emphysema patients, CXR -Classified Stage 1-4 Stage 1: FEV1>80, tx with short acting bronchodilator Stage 2: FEV1 50-79, tx with long acting B2 agonist, anticholinergic Stage 3: FEV1 30-49, tx with inhaled steroid Stage 4: FEV1 <30, tx with oxygen, pulmonary rehab
40
Describe ARDS
-Acute hypoxemic respiratory failure associated with bilateral lung infiltrates -Causes include: Pneumonia, aspiration, trauma, acute pancreatitis, inhalational injury, repurfusion injury -Symptoms include rapid onset dyspnea, tachypnea, diffuse lung crackles -Diagnosed by bilateral infiltrates on CXR, ratio of PaO2 to FiO2 <200 -Treat underlying causes, mechanical ventilation with low tidal volumes (6cc/kg), PEEP, conservative fluid management
41
Describe pulmonary embolism.
-A clot or embolus in the lungs -Risk factors: Prior PE, pregnancy, malignancy, obesity, immobility, stroke, tobacco use, recent surgery, trauma -Symptoms: Dyspnea, hemoptysis, feber, cough, tachypnea, tachycardia -Diagnosed via Wells criteria (Clinical s/s of DVT, PE diagnosis, HR >100, Immobilized x3 days, Previous PE/DVT, malignancy w/ treatment in last 6 months, hemoptysis). Also D-DImer test (only helpful to exclude in low risk patients), CTA, EKG with new right heart strain, ABG (respiratory alkalosis), V/Q (ventilation without perfusion)
42
How is a PE treated?
Heparin bridge to coumadin, INR 2-3 for 3-6 months -IVC filter -Direct thrombin inhibitors with HIT Thrombolysis or thrombectomy Contraindications to anticoagulation: Active internal bleed, aortid dissection, active hemorrhagic stroke. (Relative: thrombocytopenia, prior hemorrhagic stroke, recent internal bleed)
43
Describe acute renal failure.
An increase in serum creatinine >0.3 mg/dL over baseline Urine output less than 0.5 cc/kg/hour for more than 6-12h Can be classified as prerenal, renal, or postrenal
44
Describe differences between prerenal, renal and postrenal acute renal failure.
Prerenal: Volume depletion, severe liver disease, severe CHF. FENa (fraction excretion of sodium) <1%, ratio of BUN to creat is 10-15:1, high urine osmolarity. Treated with fluids Renal: Tubular injury, acute tubular necrosis, interstitial disease, glomerular disorder. FENa >1%, BUN to creat is 10-15:1, muddy brown casts. Tx/remove underlying agent/cause Postrenal: Urinary tract obstruction, FENa <1% oliguria/anuria, Tx remove obstruction
45
What constitutes emergent dialysis?
AEIOU Acidosis Electrolyte abrnomality Ingestion Overload Uremia
46
Describe Chronic Renal Failure
Permanent loss of renal function for at least 3 months Etiology: HTN, diabetes, renal artery stenosis, polycystic kidney disease Diagnosis: GFR <15 mL/min, albuminuria >30 mg/day Treat: Manage HTN with ACE inhibitor and angiotensin receptor blocker, low density lipoproteins (<100 mg/dL) Predictor of disease progression is proteinuria
47
How is chronic renal disease classified?
Based on GFR: >Stage G1-5. Normal GFR >90, kidney failure <15. G5D is kidney failure with dialysis Based on albuminuria: A1-A3. <30 is normal. >300 is severely increased.
48
What are potential complications (and treatments) of chronic renal failure?
Anemia (erythropoietin injections, iron) Renal osteodystrophy (phosphate binder) Hyperkalemia (dietary restriction, diuretic) Acidosis (sodium bicarbonate) Pericarditis (dialysis) Dialysis infection (antibiotics, catheter removal)
49
Describe Nephrotic Disease
Direct damage to glomeruli causing proteinuria (primary) or damage to glomeruli from systemic disease (secondary) Causes peripheral edema, hypoalbuminemia, HLD, increased proteinuria Diagnosed in urinalysis shows oval fat bodies, proteinuria, 24-h urine protein >3.5 g/day. -Primary: Membranous nephropathy, focval segmental slomerulosclerosis, goodpasture syndrome, minimal change disease (tx with ACE, steroid, cyclosporine, etc.) -Secondary: DM, MM, amyloidosis (tx underlying disease)
50
Describe nephritic disease.
Inflammatory disorder in the glomeruli Symptoms: HTN, edema, oliguria, hematuria Diagnosis: RBC casts in urine, renal biosy Can be immune complex (subacute bacterial endocarditis, post-strep, membranoproliferative) : Decreased complement levels or pauci immune (IgA nephropathy, wegner granulomatosis, CHurg Strauss syndrome): Normal complement levels
51
What are differences between ABG and VBG
ABG: Gold standard, invasive, serial exams necessary, risk of hematoma/nerve injury VBG: Easier to obtain, pH, bicarb, lactate and base excess similar to ABG
52
Describe ABG disorders
pH= HCO3/CO2 Metabolic acidosis: Decreased HCO3 vs Metabolic alkalosis Increased HCO3 Respiratory Acidosis: Increased PaCO2 vs respiratory alkalosis decreased PaCO2 Compensatory change is opposite once you determine the primary disorder
53
How do you calculate anion gap?
Na- (Cl+HCO3) <12
54
What are causes/tx of metabolic acidosis
AG (MUDPILES): Methanol, uremia, diabetic ketoacidosis, paralehyde ingestion, isoniazid, lactic acidosis, ethylene glycol ingetion, salicylate ingestion Non AG: Diarrhea, renal loss Tx underlying causes and sodium bicarbonate
55
What are the causes/tx of metabolic alkalosis?
Adrenal disorders increasing reabsorption of bicarb, extracellular fluid contraction, diuretics Tx underlying cause, normal saline with potassium, consider spironolactone
56
What are the causes/tx of respiratory acidosis?
Hypoventilation, COPD, brainstem injury, muscle fatigue, drug overdose Tx w/ supplemental oxygen, tx underlying disorder, consider mechanical ventilation
57
What are the causes/tx of respiratory alkalosis?
Hyperventilation, anxiety, sepsis, pregnancy, liver disease, asthma Tx: Underlying disorder, inhale CO2
58
Describe hyponatremia.
Normal 135-145 Symptoms: Lethargy, seizures, nausea/vomiting, confusion Diagnosis: Measure serum osmolarity Normal (Hyperlipidemia, hyperproteinemia). High (hypertonic hyponatremia, hyperglycemia), low (hypotonic hyponatremia, hypovolemic salt loss, euvolemic SIADH, hypervolemic CHF liver/renal failure) Tx: Rapid normalization can lead to demyelinating encephalopathy, treat volume status and neurologic symptoms
59
Describe hypernatremia
-Lethargy, wakness, irritability, seizure, polyuria -Measure volume status (renal loss of water and not sodium from renal failure), diabetes insipidus (loss of water only), cushing syndrome (excess mineralcorticoids and sodium production) Tx: Calculate water deficit and replace with isotonic fluid, treat DI (w/ vasopresin)
60
Describe potassium disorder workup
Normal 3.5-5 Urine potassium and chloride level, serum mag, ABG
61
Describe hypokalemia
Hypo is better than hyper Non renal loss fro mdiarrhea renal loss can be from magnesium depletion, diuretic, NG suctioning, Alkalosis -Symptoms: Muscle weakness, abnormal EKG with flattening and inversion of T waves and QT prolongation -Treat: Underlying cause, Mag replacement, KCl gradually
62
Describe hyperkalemia
-Causes acidosis or rhabdomyolysis, or adrenal insufficiency, drugs, renal insufficiency -EKG changes: Peaked T wave, flattened P, increased PR, disappeared P wave, QRS prolongation. Eventually ventricular asystole -Respiratory failure, nausea/vomiting, muscle weakness -Tx: IV calcium gluconate to decrease cardiac excitability, insulin/dextrose (K goes into cell), diuretics, dialsysis
63
Describe Crohn disease
-Chronic, GI (irritable bowel syndrome) with patchy trasmural inflammation non-bloody diarrhea, low grade fever, anywhere in GI tract (mostly ileum) diagnosed with colonoscopy/biopsy Tx with steroid, immunomodulary drug, 5-aminosalicylic acid
64
Describe ulcerative colitis
-Chronic, GI (IBS) with diffuse continuous mucosal inflammation Blood diarrhea, located in colon to rectum Colonoscopy with stool study, lead pipe on xray Increased malignancy Tx with mesalmine, steroid, surgery
65
Describe Hepatitis A
Liver disease diagnosed via antihepatitis antibody. Fecal or oral transmission. Treated with supportive care
66
Describe Hepatitis B
Liver disease diagnosed via surface antigen (active) vs antihepatitis antibody (prior) Blood to blood transmission Tx: Follow LFT and treat as necessary. Liver transplant at end stage
67
Describe Hepatitis C
Liver disease diagnosed with antihepatitis antigen or PCR Blood to blood tramission Treated with medication (interferon, ribavirin), transplantation at end stage
68
Describe GERD
Stomach acid back-flow from lower esophageal sphincter relaxation Retrosternal burning, regurgitation Treat empirically, but can do upper endoscopy with biopsy Elevate head of bed, stop tobacco/alcohol diet modification, antacids, histamine blockers, PPI Could be complicated to Barrett's esophagus, adenocarcinoma, upper GI bleed, cough, asthma
69
Describe ESLD (end stage liver disease)
-Chronic hepatocellular injury leading to fibrosis of the liver -Symptoms: fatigue, anorexia, melena, spider nevi, jaundice, hand tremor, telangictasia -Diagnosis: LFT, liver biopsy, monitor with MELD (model for end stage liver disease) score or Child-Turcotte-pugh score -Treatment: Avoid alcohol, liver metabolized meds, tx underlying disease process, monitor for hepatocellular carcinoma Complications: Esophageal varicies, ascites, increased bleeding, portal hypertension, hepatic encephalopathy
70
What is the Child-Turcotte-Pugh Score?
For ESLD. 5-6 points 90% 3 year survival, 7-9 points 50-60% survival, >9 points 30% 3 points each (ascites, encephalopathy, albumin, prothrombin time, bilirubin)
71
Describe microcytic anemia
Anemia with MCV <80 fL -Iron deficiency anemia -Symptoms: Pica, ice chip cravings, glositis -Tx with iron therapy
72
Describe normocytic anemia
Anemia with MCV 80-100 (mean corpuscular value) -Renal insufficiency anemia, seen when anemia noted with underlying renal disorder -Tx with Erythropoietin admin, iron dosing
73
Describe macrocytic anemia
Anemia with MCV >100 -B12/folate deficiency -Glossitis, atrophic gastritis, neuro symptoms -Tx with B12/folate
74
What is hyperproliferative (high reticular cell count) anemia
RBC destruction in bloodstream (schistocytes, G6PD deficiency), spleen (spherocytes) or from blood loss
75
Describe Sickle Cell Disease
-Homozygous defect in gene for beta-globulin that produces hemaglobin S -Diagnosed via target cells, sickle cells, howell-jolly bodies, hemaglobin S -Can be triggered by dehydration, acidosis or hypoxia -Can present with acute chest pain,s troke, autosplenectomy -Tx w/ folate, hydroxyurea, hydration, O2, transfuse for major surgery Acute complications: Stroke, splenic infarct, osteomyelitis Chronic complications: Retinopathy, avascular necrosis of hip, chronic renal failure
76
What is hemophilia A?
A bleeding disorder with Factor 8 deficiency. Patients noted to have spontaneous bleeding. Treated with desmopressin or factor replacement
77
What is hemophilia B?
A bleeding disorder with Factor 9 deficiency. Patients noted to have spontaneous bleeding, prolonged PTT. Treat with factor replacement
78
What is von Willebrnad disease?
Bleeding disorder with decreased von Willebrand factor and factor 8 deficiency. Patients noted to have petechiae, mucosal bleeding, epistaxis. Treat with desmopressin, aminocaproic acid or factor 8 replacement
79
What is immune thrombocytopenia purpura?
An immune condition characterized by a normal spleen with petechiae and mucosal bleeding due to immune destruction of platelets. Treat with platelet transfusions if drops below 25-30k
80
What is disseminated intravascular coagulation (DIC)
Consumptive coagulopathy associated with serious illness. Thrombocytopenia with excessive bleeding or clotting -Dx: decreased fibrinogen, platelets, increased PT or PTT -Tx: Underlying cause, platlets, cryoprecipitate for bleeding, low dose heparin for clotting
81
What are conditions that cause a hypercoagulable state?
Prior embolus, pregnancy, surgery, tobacco, prolonged immobilization, hospitalization, malignancy. -Also Factor V leiden (venous thrombus), protein C/S deficiency (vein or artery), heparin induced thrombocytopenia (vein or artery) Noted on CBC, PTT Treat INR 2-3 x3-6 months
82
Lab check/reversibility of warfarin
-INR -FFP, VItamin K
83
Lab check/reversibility of heparin?
-PTT and platelet count -Protamine
84
Lab check/reversibility for low molecular weight heparin
-Antifactor Xa -No reversibility
85
Lab check/reversibility of fondaparinus (factor Xa inhibitors)
-No monitoring -No reversibility
86
Lab check/reversibility for dabigatran (direct thrombin inhibitor)
-PTT -No reversibility
87
Describe diabetes mellitus.
A disease characterized by type I or type II DM Type I: Autoimmune islet cell destruction leading to insulin deficiency. Symptoms include polyuria, polydipsia (excessive thirst), polyphagia (excessive hunger). Treated with insulin therapy and glycemic control Type II: Insulin resistance associated with obesity. Treated with oral hypoglycemic/glycemic control. Long term complications: Retinopathy, neuropathy, infections, MI, stroke Short term: Diabetic ketoacidosis (Type I), hyperosmolar nonketotic come (type II)
88
Describe the different types of insulin therapy?
Ultra short acting (lispro): peak 60-90 min Short acting (regular) 1-3 hr Intermediate (NPH) 8-10 hr Long acting (glargine): Lasts 24h
89
Describe different types of oral hypoglycemics
Metformin: Decreases insulin resistance and glucose production, can cause lactic acidosis, GI upset Sulfonurea: Stimulates insulin release, can cause hypoglycemia Repaglinide: Stimulates pancreas to release insulin. Can cause weight gain Pioglitazone: Decreases insulin resistance peripherally, causes fluid retention
90
Describe diabetic ketoacidosis
An insulin deficiency and glucagon excess that causes severe hyperglycemia and ketogenesis. Hyperglycemia causes osmotic diuresis leading to dehydration and volume depletion. Symptoms: abdominal pain, nausea, kussmaul respirations (deep, acidodic labored breathing), ketone breath, altered consciousness Diagnosed: Glucose >250, metabolic acidosis with anion gap, ketones (hyperkalemia, hyponatremia) Tx: IV insulin drip, manage Na, K, Mg
91
Describe hypothyroidism
Endocrine disease characterized by increased TSH and decreased T4 Symptoms of fatigue, weight gain, cold intolerance, depression Ex: Hashimoto's, subacute thyroiditis, iodine deficiency Tx w synthroid Complications: Myxedema coma w/ hypercapnia, hypoventilation, hypothermia
92
What is addison disease?
Addison disease is a primary adrenal insufficiency caused by autoimmune adrenalitis, malignancy or infection Symptoms include hyperpigmentation of the oral mucosa, dehydration, hypotension, fatigue Diagnosis by low cortisol, high ACTH Treat with mineralcorticoid and glucocorticoid replacement
93

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