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Internal Medicine General > Deck 2 > Flashcards

Deck 2 Flashcards

1
Q

What disease has positive–

  1. ANA (anti nuclear antibodies)
  2. Anti histone antibodies
  3. Anti-dis-DNA antibodies?
A
  1. Sensitive lupus
  2. Specific drug induced lupus
  3. Specific lupus + renal involvement
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2
Q

What disease has positive–
1 anti smooth muscle antibodies
2. Mitochondrial antibodies
3. Centromere antibodies

A
  1. Autoimmune hepatitis
  2. PBC
  3. Scleroderma
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3
Q

Which disease has positive–

  1. Anti Ro+La antibodies
  2. Anti CCP antibodies
  3. Anti RF antibodies
A
  1. Sjogrens
  2. RA
  3. RA
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4
Q

What disease has positive–

  1. Anti jo antibodies
  2. Topoisomerase antibodies
A
  1. Polymyositis

2. Systemic scleroderma

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5
Q

Risk factors for heart disease

A 
DM
Smoking
HTN
Dyslipidemia 
Family history
Central obesity
Cocaine use
Sedentary lifestyle
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6
Q

What are risk factors for PE

A 
Cancer
Exogenous hormones
Recent surgery
Recent immobility including long travel
Hypercoagulable states (pregnancy, clotting disorders)
History of PE or DVT
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7
Q

What is the differential for sharp pleuritic pain?

A

Pneumothorax
Pulmonary embolism
Pericarditis (also positional)

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8
Q

What are the life threatening causes of chest pain that you would want to rule out?

A 
PE
MI
Dissection
Tamponade 
CHF
Pneumothorax
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9
Q

What is the differential for visceral chest pain (aching, poorly localized)

A

Myocardial ischemia
–> worrisome features are prolonged pain of more than 20 min and rest pain

Aortic dissection–abrupt, intense pain (often “tearing”)

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10
Q

What is the pathological change behind stable angina and what is its clinical presentation

A

Luminal narrowing

Central chest discomfort worsened by exertion, emotion and eating
Relieved by rest and nitro

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11
Q

What is the pathological change behind unstable angina and what is the clinical presentation

A

Plaque rupture or thrombus

Worsening pattern or rest pain
No elevation in troponin, with or without ECG changes of ischemia

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12
Q

What is the pathological change behind an NSTEMI and what is the clinical presentation

A

Partial occlusion

Non ST elevation MI–elevation in troponin with or without ECG changes of ischemia

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13
Q

What is the pathological change behind a STEMI and what is the clinical presentation?

A

Complete occlusion

ST elevation MI–elevation in troponin, with distinct ST segment elevation in more than two continuous leads, new LBBB or posterior wall MI with reciprocal ST depression in pre cordial leads on ECG

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14
Q

What is the cardiac Ddx for chest pain

A

Myocardial–> MI, angina, myocarditis

Valvular–> aortic stenosis–> CHF

Pericardial–> pericarditis, tamponade

Vascular–> aortic dissection

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15
Q

What is the pulmonary Ddx for chest pain?

A

Airway–> obstructive (COPD, asthma)

Parenchyma–> pneumonia

Pleural –> Pleuritis, pneumothorax, pneumomediastinum, pleural effusion

Vascular–> pulmonary embolism

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16
Q

What is the GI ddx for chest pain

A 
Esophagitis
Esophageal cancer
Gastritis
PUD
Pyloric stenosis
Cholescystitis 
Pancreatitis
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17
Q

Other than cardiac, pulm, GI, what is also on the Ddx for chest pain?

A

MSK –>chostochondritis

Shingles

Anxiety/panic

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18
Q

What should you ask for on history for chest pain?

A
  1. Characterize the chest pain–> location, onset, provocation/palliation, radiation, severity, timing
  2. Ask about specific patterns of pain for AoD, PE, MI
  3. Associated symptoms–> dyspnea, palpitations, diaphoresis, syncope, nausea
  4. Infectious symptoms–> fever chills, headache, fatigue, cough, sputum
  5. Precipitating factors–> comforting, exertion, trauma
  6. Meds
  7. Risk factors for CHD and PE
  8. ROS–> B symptoms, N/V/D, abdo pain, GU sx
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19
Q

What type of process presents typically with mid sternum pain radiating to back, sudden onset, tearing, progressive?

A

Aortic dissection

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20
Q

What type of process presents typically with heavy pressure chest pain, retrosternal, comes on suddenly and lasts hours, radiates to arm/jaw/shoulders, and is relieved by nitro?

A

MI

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21
Q

What type of process presents typically with pleuritic, sudden onset chest pain that is severe and one sided with dyspnea?

A

PE

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22
Q

What signs on physical exam would suggest AoD?

A
  1. Discrepancy in pulse between arms of more than 20 systolic or more than 10 diastolic
  2. New aortic regurgitation murmur
  3. Absent or reduced pulses
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23
Q

What does a pericardial rub suggest?

A

Pericarditis

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24
Q

What does a new aortic regurgitation murmur on exam indicate?

A

Aortic dissection

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25
Q

What does pulsus paradoxus indicate?

A

More than 10

Asthma or tamponade

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26
Q

What does absent or reduced pulses indicate?

A

Aortic dissection or emboli

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27
Q

What might a new mitral regurgitation murmur indicate in the setting of CP?

A

Papillary muscle dysfunction secondary to ischemia

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28
Q

What does Becks triad indicate? What is Becks triad?

A

Tamponade

Muffled heart sounds
Hypotension
Elevated JVP

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29
Q

What might a loud S2 indicate in the setting of chest pain?

A

Indicates acute elevation in right sided pulmonary pressure

In the setting of chest pain, suggestive of a PE

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30
Q

What does decreased air entry to one side on auscultation of the lungs suggest?

A

Pneumothorax

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31
Q

What might be the pathological process in a patient with chest pain plus:
Hypotension
Elevated JVP
Displaced trachea

A

Tension pneumo

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32
Q

What might be the pathological process in a patient with chest pain plus
Egophony
Decreased air entry
Dullness to percussion

A

Pneumonia or pleural effusion

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33
Q

What might a pleural rub indicate?

A

Pneumonia or PE

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34
Q

Describe a physical exam approach to chest pain

A

General appearance–apprehension, diaphoresis, pallor, cyanosis, anxiety

Vitals–different BP in arms, pulsus paradoxus, absent or reduced pulses

CV–murmur, pericardial rub, Becks triad, S3, loud S2

Resp–air entry bilaterally, dullness or hyperresonance to percussion, midline trachea, ego phone, pleural rub

Abdo–referred pain or diaphragm irritation

MSK–chest wall tenderness

Skin–zoster

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35
Q

What dermatological condition can cause chest pain?

A

Zoster can cause severe pain before onset of rash

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36
Q

What labs should be ordered in the setting of chest pain, and why are you ordering each?

A
  1. Baseline–CBC, lytes, urea, Cr, glucose
  2. Cardio–troponin and repeat, BNP
  3. Resp–d dimer
  4. Infection–CRP, LDH
  5. LFTs if indicated by Hx/physical (I.e is suspect referred pain from cholescystitis, etc)
  6. ABG–normal ABG does not rule out PE
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37
Q

What investigations should be done in the setting of CP and why would you do each?

A
  1. ECG–MI, pericarditis
  2. CXR–pneumothorax, pneumonia, CHF
  3. Echo–tamponade, valvular disease
  4. CT angio–PE (coronary angiography for CAD)
  5. VQ scan–PE if patient has kidney disease and cannot tolerate contrast
  6. MIBI–ACS
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38
Q

What may be components of treatment of any cause of chest pain?

A

ABC protection

Cardiac monitor, pulse ox, IV access, O2 provided/made available

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39
Q

How would you treat acute MI?

A

Admit CCU

Oxygen
ASA
IV nitro 
IV beta blocker 
LMWH
clopidogrel
Thrombolysis 
angioplasty 
Consider GIIb/GIIa inhibitors
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40
Q

How would you treat unstable angina/ACS?

A

Admit CCU or monitored bed

Oxygen 
ASA
IV nitro
IV beta blocker 
LMWH
?clopidogrel
?angioplasty 
Consider GIIb/GIIa inhibitors
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41
Q

How would you treat tension pneumothorax?

A

Admit thoracic surgery

Needle aspiration or thoracostomy

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42
Q

How would you treat PE?

A

Admit medicine or ICU/thoracic surgery

IV/LMWH and oxygen
Directed thrombolysis or consider embolectomy in extreme cases

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43
Q

How would you treat cardiac tamponade?

A

Admit CCU

Pericardiocentesis

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44
Q

How would you treat esophageal rupture

A

Admit ICU/thoracic surgery

Fluids
IV abx
Emergency surgery

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45
Q

How would you treat AoD?

A

Admit ICU or thoracic surgery or Admit CCU

Type A–> ascending aorta
Surgery

Type B–> arch or descending aorta
Medical control of HTN with negative inotropes
Surgery if necessary

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46
Q

How would you treat severe pneumonia?

A

Admit medicine/ICU

IV abx and oxygen

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47
Q

How would you treat GI causes of CP including esophageal spasm or reflux

A

Discharge and follow up with GP

Symptomatic treatment

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48
Q

How would you treat a simple pneumothorax

A

Discharge–follow up in ED for repeat CXR and reassessment

Observe or needle aspiration

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49
Q

How would you treat a simple pneumomediastinum

A

Discharge and follow up as warranted

Observe/investigation of cause

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50
Q

How would you treat an uncomplicated pneumonia?

A

Discharge and follow up with GP

Oral Abx

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51
Q

How would you treat pericarditis?

A

Admit medicine if complicated otherwise discharge and follow up with GP

Treat underlying cause if present

It post viral, NSAIDs and steroids

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52
Q

How would you treat MSK/cervical/thoracic radicular causes of CP?

A

Discharge and follow up with GP

Symptoms treatment

NSAIDs, acetaminophen, adjunctive therapies

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53
Q

How would you treat herpes zoster?

A

Discharge and follow up with GP

Anti virals if lesion onset was within 48-72 hours

Symptom treatment with NSAIDs, acetaminophen, narcotics

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54
Q

What are the symptoms of HUS/TTP, DIC?

A

FAT RN 2

Fever
Anemia
Thrombocytopenia 
Renal impairment 
Neuro impairment

2 of the above are required for an immediate smear

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55
Q

What can cause folic acid deficiency

A

Diet or drugs (methotrexate)

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56
Q

What pattern on serum iron, TIBC, ferritin would suggest:

Iron deficiency anemia

A

Low iron
High TIBC
Low ferritin

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57
Q

What pattern on serum iron, TIBC, ferritin would suggest:

Thalassemias

A

Normal iron
Normal TIBC
Normal ferritin
In the setting of a macrocytic anemia

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58
Q

What pattern on serum iron, TIBC, ferritin would suggest:

Anemia of chronic disease

A

Low iron
Low TIBC
High ferritin

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59
Q

What pattern on serum iron, TIBC, ferritin would suggest:

Sideroblastic anemia

A

High iron
Normal TIBC
Normal or high ferritin

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60
Q

What causes pre-renal injuries?

A
  1. True intravascular fluid loss
  2. Decreased effective circulating volume
  3. Impaired renal perfusion
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61
Q

What types of processes cause true intravascular fluid loss?

A

Blood loss
Renal or GI losses
Inadequate oral intake
Insensible losses (fever, burns)

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62
Q

What types of processes cause decreased effective circulating volume?

A

CHF
Hypoalbuminemia–nephrotic syndrome, cirrhosis, malnutrition
Shock–distributive or cardiogenic

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63
Q

What types of processes cause impaired renal perfusion?

A
  1. Macro vascular–> RAS, dissection, thrombus

2. Micro vascular–> NSAIDs (afferent vasoconstriction), ACEi (efferent vasodilation), hypercalcemia

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64
Q

What are the three areas of the kidney that can be injured causing renal AKI?

A

Glomerulus
Tubular
Interstitial
Vascular

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65
Q

What are the parts of the glomerulus than can be injured in renal AKI?

A 
Glomerular capillary wall
Endothelium
Basement membrane
Podocytes
Mesangium
Bowman's space and capsule
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66
Q

How are glomerular injuries (causing AKI) clinically divided?

A

Nephrotic syndrome and nephritic syndrome

Can also classify by pathology on renal biopsy and by primary versus secondary

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67
Q

What are the clinical features of nephritic syndrome?

A
  1. HTN
  2. Active sediment (RBC casts, dysmorphic RBCs)
  3. Variable proteinuria (including in the nephrotic range)
  4. Oliguria (less than 400 mL per day)
  5. Varying renal insufficiency
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68
Q

What are the pathological processes behind nephritic syndromes?

A
  1. Linear–> anti glomerular basement membranes disease, Goodpastures disease
  2. Immune complex–>
    - Primary–>IgA nephropathy, membranoproliferative glomerular nephritic
    - Secondary–>SLE, HBV, post strep GN, IE, cryoglobulinemia
  3. Pauci-immune (ANCA+ vasculitis)–> GPA (PR3+), MPA (MPO+), EGPA (Churg-Strauss) (MPO+)
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69
Q

What are the clinical features of nephrotic syndrome? There is a mnemonic.

A

PALE

  1. Proteinuria more than 3.5 g/day
  2. HypoAlbuminemia
  3. HyperLipidemia
  4. Edema

Also–
Hypercoagulable (loss of protein C and S, anti thrombin)
Immunosuppression (lose immunoglobulin)
Bland sediment (fatty casts, oval fat bodies)
GFR usually preserved

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70
Q

What are the histopathological classifications of nephrotic syndrome?

A

Focal segmental glomerulosclerosis
Membranous nephropathy
Minimal change disease
Membranoproliferative GN

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71
Q

What are some secondary causes of nephrotic syndrome?

A 
DM
Obesity
Autoimmune (SLE, RA)
Infectious (Hep B, C, HIV, EBV, syphilis)
*Drugs (NSAIDs, lithium, heroin)
*Malignancy
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72
Q

What is RPGN-rapidly progressive glomerulonephritis?

A

Clinical syndrome manifested by progressive loss of renal function over days/weeks

Must have features of glomerular disease in urine

Often presents as nephritic syndrome of rapid onset

Anti GBM, immune complex, pauci-immune can present as RPGN

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73
Q

What are the two types of tubular injuries seen in AKI?

A
  1. ATN

2. Intra tubular obstruction

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74
Q

What causes ATN?

A
  1. Ischemia–> prolonged pre renal insult
  2. Toxic–> drugs (contrast dye, aminoglycosides, acyclovir), pigment (hemoglobin, myoglobin), protein (myeloma light chains)
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75
Q

What causes intra tubular obstruction in tubular injury in AKI?

A
  1. Crystals–irate, calcium oxalate, drugs like methotrexate
  2. Protein–myeloma light chains
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76
Q

How do you distinguish tubular from pre renal AKIs?

A
  1. Rate of rise of creatinine is faster ATN
  2. Pre renal will respond to a fluid challenge within the first 24-72 hours
  3. The fractional excretion of sodium is less than 1% in pre renal and more than 2% in ATN
  4. Urine sodium is less than 20 in pre renal and more than 20 in ATN
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77
Q

What are the 5 Is of acute interstitial kidney injuries?

A

Infection –> bacterial (staph, strep..), viral (CMV, EBV, HIV), fungal

Inflammation –> sjogren’s, SLE, IgG4, GPA

Infiltration–> sarcoidosis, TB (usually chronic/progressive), lymphoma

Iatrogenic –> NSAIDs, Abx (penicillins, Sulfa), diuretics, PPI, allopurinol

Idiopathic

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78
Q

What is the classic triad of acute interstitial nephritis?

A

Fever
Rash
Eosinophilia

With or without eosinophils (poor sens and spec)
With or without WBC casts and sterile pyuria

Typically non oliguric (pee normal amount)

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79
Q

What types of vascular processes can cause an AKI?

A
  1. MAHAs–> TTP/HUS, malignant hypertension, APLAS
  2. Embolic phenomena–> cholesterol, atheroembolic
  3. Vasculitis–> PAN, takayasu’s
80
Q

What can cause a post-renal injury resulting in an AKI?

A
  1. Urethra–> stricture, stenosis
  2. Prostate–> BPH, prostatitis, cancer
  3. Bladder–> cancer, stone, clot, neurogenic
  4. Ureters–>
    - intra luminal–> cancer, stone, clot
    - extra luminal–> cancer, pregnancy, retroperitoneal fibroids
81
Q

What are some questions to ask on history to investigate pre renal causes of AKI?

A

Recent N/V/D/blood loss

Hx CHF, cirrhosis

Use of NSAIDs, ACEi, cocaine

82
Q

What are some questions to ask on history to investigate possible post renal causes of an AKI?

A

Urinary frequency, urgency, nocturnal, dribbling, hematuria

History of stones, BPH, prostate cancer

Constitutional sx

83
Q

What are some questions to ask on history to investigate a glomerular cause of an AKI? Why would you ask each of them (what are you hoping to rule in or out)?

A
  1. Frothy urine–> proteinuria
  2. Hematuria or cola coloured urine
  3. Recent URTI/strep throat–> post strep GN
  4. Alopecia, oral ulcers, face rash, arthralgias–> SLE
  5. Fevers, IE risk factors–> IE
  6. History of HBV, HVC or risk factors
  7. Family history of GN/IgA nephropathy (especially of Asian descent)
  8. Hemoptysis–> pulmonary renal syndromes like GPA
84
Q

What does frothy urine suggest?

A

Proteinuria

85
Q

What symptoms suggest SLE?

A 
Alopecia
Face rash
Oral ulcers
Arthralgias
Renal injury
86
Q

What questions would you ask on history to investigate Renal tubular causes of an AKI?

A
  1. Drug history–aminoglycosides, acyclovir, amphoteracin (ATN)
  2. Radio contrast exposure (ATN)
  3. Gout, malignancy history (urate nephropathy)
  4. “Found down” or muscle injury (pigment nephropathy)
87
Q

What questions would you ask on history to investigate renal interstitial causes of AKI?

A
  1. Recent or current infection
  2. Drug history –Abx, NSAIDs, diuretics, PPI, allopurinol
  3. Rheumatological review of systems (Sjogren’s, SLE)
88
Q

What questions would you ask on history to investigate renal vascular causes of AKI?

A 
Bloody diarrhea (HUS)
Etc.
89
Q

What are some consequences of AKI that you would want to investigate on history?

A

Symptoms of volume overload–dyspnea, Orthopnea, PND, peripheral edema

Decreased urination–oliguria or anuria

Nausea, malaise, confusion, pleuritic CP (pericarditis), bleeding (uremia)

90
Q

What should you look for in particular on physical exam of the patient with an AKI?

A

General inspection

Vitals–> hypertension (nephritic syndromes), fevers (IE, pyelonephritis), hypoxemia

Neuro–> orientation, asterixis

H&N–> throat exam (post strep GN), alopecia/facial rash/oral ulcers (SLE)

Respiratory–> crackles (volume overload, pulm hemorrhage)

CV–> JVP, peripheral edema, mucous membranes (volume status–IMPORTANT), new murmur (IE), pericardial rub (pericarditis)

Abdo–> CVA tenderness (pyelonephritis), DRE (BPH, prostate cancer)

Derm–> generalized excoriations, rash (AIN, cryoglobulinemia, vasculitis)

MSK–> arthritis/arthralgias (SLE, gout)

Lymph nodes–> infections and malignancy

91
Q

What investigations would you order to assess an AKI?

A
  1. General
  2. UA and micro–> consider urine C&S, urine Na and FENa
  3. Renal U/S with or without foley insertion
92
Q

What are the important findings on UA in an AKI?

A

Proteinuria
Positive heme–> hemoglobinuria, myoglobinuria, hematuria
Positive leukocyte esterase–> pyelonephritis or AIN

93
Q

If you see Uric acid crystals on urine microscopy, what disease are you thinking

A

Uric acid nephropathy

94
Q

If you see calcium oxalate on urine microscopy, what are you thinking?

A

Ethylene glycol poisoning

95
Q

If you see dysmorphic RBCs on urine microscopy what are you thinking?

A

Glomerulonephritis

96
Q

If you see isomorphic RBCs on urine microscopy what are you thinking?

A

Stones, malignancy, IgA, TBMD

97
Q

If you see no RBCs on urine microscopy but positive heme on dipstick, what are you thinking?

A

Hemoglobinuria from TTP/HUS or myoglobinuria from rhabdomyolysis

98
Q

If you see WBCs on urine micro, what are you thinking?

A

Infection

Interstitial nephritis

99
Q

What do hyaline casts indicate on urine micro?

A

Common and NON SPECIFIC

Can be a sign of volume depletion

100
Q

What do RBC casts indicate on urine microscopy?

A

Glomerulonephritis

101
Q

What do WBC casts indicate on urine micro?

A

Interstitial nephritis

Pyelonephritis

102
Q

What do heme granular casts indicate on urine micro?

A

“Muddy brown casts”

ATN

103
Q

What do fatty casts indicate on urine micro?

A

Found with significant proteinuria like in nephrotic syndrome

104
Q

What does a FeNA of less than 1% indicate?

A

Tubules are still functioning and reabsorbing sodium

Pre renal cause of AKI

105
Q

What does a FeNA or more than 1% indicate?

A

Sodium not being maximally resorted

ATN or non volume depletion cause

106
Q

What’s the best way to determine if you patient has a pre renal AKI?

A

Fluid challenge

107
Q

Tests for SLE

A

ANA
C3
C4

108
Q

Tests for post infectious strep

A

ASOT

109
Q

Tests for IE

A

Blood cx

110
Q

Tests for cryoglobulinemia

A

Crayons

HCV

111
Q

Tests for membranoproliferative glomerulonephritis

A

HBV
HCV
HIV

112
Q

Tests for anti-GBM disease

A

Anti GBM antibody

113
Q

Tests for GPA, MPA, Churg Strauss

A

ANCA

114
Q

Tests for multiple myeloma

A

SPEP and UPEP

115
Q

What are the 5 golden rules of AKI management?

A
  1. Give fluids if dry–> pre renal management
  2. UA and micro–> renal investigation
  3. Stop nephrotoxic drugs, really dose meds–> all causes
  4. Insert foley–> post renal management
  5. Order renal U/S to rule out hydro–> post renal suspicion
116
Q

What are the acute indications for dialysis? There is a mnemonic.

A

AEIOU

Acidosis–> refractory metabolic acidosis

Electrolytes–> refractory hyperkalemia

Ingestion–> methanol, ethylene glycol

Overload–> refractory volume overload

Uremia–> pericarditis, encephalopathy, asterixis, seizures

117
Q

What is the basic diagnostic approach to AKIs?

A

Pre renal
Renal
Post renal

118
Q

What is the basic process of AKI evaluation and work up

A

Hx, Physical, Basic labs
UA and micro
Fluid challenge
Insert foley and get renal U/S
Stop nephrotoxic drugs and renal dose meds
Evaluate for acute indications for dialysis (AEIOU)

119
Q

What is normal body temp?

A

36.8 +/- 0.4 degrees

120
Q

What is defined as fever?

A

Higher than 37.2 in AM

Higher than 37.7 in PM

121
Q

What is the definition of fever of unknown origin? What are the types?

A

More than 38.3 on several occasions over a defined period with us revealing investigations

  1. Classic–> lasting more than 3 weeks, where 3 outpatient visits, 3 days in hospital or 1 week of ambulatory testing revealed no cause
  2. Nosocomial–> 3 days of investigations and 2 days of Cx with no growth
  3. Neutropenic–> 3 days of investigations and 2 days culture with ANC less than 0.5
  4. HIV associated
122
Q

Define fever and state the physiological changes fever causes

A

Elevation of body temp with elevation in hypothalamic set point

Causes peripheral vasoconstriction–> patient feels cold
Heat production mechanisms are activated–> shivering
Nonspecific myalgias and arthralgias

123
Q

What is hyperthermia and how does it differ from fever

A

Increased body temp not due to pyrogens (no increase in hypothalamic set point)

124
Q

What is the Ddx of classic FUO?

A

Infection
Neoplasm
Inflammatory disease–> systemic rheum disease, vasculitis, granulomatous disease
Misc–> PE, drug fever, hereditary fever syndrome, hypothalamic dysregulation

125
Q

What is the Ddx of nosocomial FUO?

A 
Infection (catheter, c diff, sinusitis)
No infectious (drug fever, PE, cholescystitis)
126
Q

Ddx of neutropenic FUO

A

More than 60% of patients with febrile neutropenia are infected and 20% are bacteremic

Candida and aspergillosis are common

127
Q

Ddx of HIV associated FUO

A

More than 80% are infected

128
Q

What should you be asking about on Hx in a patient with FUO

A 
Particular attention to chronology 
Meds
Pet exposures
Sick contacts
Sexual contacts
Travel
Trauma
Malignant symptoms
129
Q

What should you focus on in physical exam in a patient with FUO

A

General complete physical exam looking for infectious or malignant symptoms

Precise rash description if present

130
Q

What should you order in terms of investigations for FUO

A 
CBC and diff
Lytes
BUN/Cr
LFTs
ESR/CRP
UA
Infectious workup--> HIV, CMV, EBV, TB skin test, VDRL
Autoimmune--> ANA, RF
Cultures--> urine, blood, sputum
Malignant--> SPEP, UPEP
If indicated by sx--> CXR, AXR
131
Q

How do you treat FUO?

A

Treat underlying cause
Antipyretics–> aspirin, NSAIDs, glucocorticoids
If patient is hyperpyretic use cooling blankets

132
Q

Name some agents commonly associated with drug induced fever

A 
Allopurinol 
Captopril
Erythromycin
Heparin
HCTZ
Isoniazid 
Nifedipine 
Penicillin 
Phenytoin 
Procainamide
Quinidine
133
Q

What is the most common cause of decreased renal function in hospitalized patients

A

Pre renal

134
Q

Why do you get elevated urea in pre renal AKI

A

Enhanced tubular absorption of both sodium and water increases passive reabsorption of urea

135
Q

What is the most common type of intrinsic renal failure?

A

ATN

136
Q

What is the leading cause of intrinsic renal injury in hospitalized patients

A

Sepsis

Next most common is renal ischemia during major heart surgery or vascular surgery

137
Q

What is the most common cause of acute interstitial nephritis

A

Allergic reaction to drug

Look for fever, drug rash, eosinophilia or renal dysfunction

Commonly fluoroquinolones, Sulfa drugs, beta lactams, NSAIDs

138
Q

How does NSAID associated interstitial nephritis usually present

A

As nephrotic syndrome

139
Q

How do ACEi cause renal injury?

A

Efferent vasodilation which causes decrease in filtration pressure

140
Q

What drugs are know to cause efferent arteriole vasoconstriction in the kidney

A

Amphoteracin B
Cyclosporine A
NSAIDs
Radio contrast

141
Q

What types of cells and casts will be seen in ATN

A

Renal tubular epithelial cells

Granular and muddy brown casts

142
Q

What type of cells and casts will be seen in acute glomerulonephritis

A

Dysmorphic RBCs
RBCs
WBCs
Epithelial cells

RBC

143
Q

What types of cells and casts are seen in acute interstitial nephritis (AIN)

A

Eosinophils
WBCs

WBC and hyaline

144
Q

What are the symptoms of hypercalcemia

A

Bones, stones, groans, moans, psychiatric overtones + dehydration

Bone pain
Kidney stones
Abdo pain
Psych presentation

Dehydration because hypovolemic because calcium is an active osmole

145
Q

How do you treat hypercalcemia

A
  1. Fluids–make them pee it out, works right away
  2. Treatment for malignant hypercalcemia is bisphophonates like PAMINDRONATE once you have normalized the calcium level (inhibit osteoclasts resorption of bone)
  3. Imaging to work up mets if malignant

Loop diuretics increase calcium excretion and work right away
Calcitonin SC can inhibit bone resorption and works within hours
Surgery for primary hyperparathyroidism

146
Q

Describe and approach to hypercalcemia

A

Either high PTH or low PTH then go from there

147
Q

What is the Ddx of hypercalcemia with low PTH

A
  1. MALIGNANCY–> breast, lung, colon, kidney, prostate and multiple myeloma
    - -on Hx ask about risks for these cancers
  2. Vitamin D excess
  3. Thiazides
  4. Milk alkali syndrome
  5. Increased bone turnover states–> ie Paget’s disease
148
Q

What is the Ddx of hypercalcemia with high PTH?

A
  1. HYPERPARATHYROIDISM
    Primary versus tertiary–> tertiary is in renal patients that have had high PTH for so long that is becomes autonomous
  2. Familial hypocalciuric hypercalemia (FHH)–> don’t pee out calcium
149
Q

What is the mechanism behind malignant hypercalcemia

A
  1. Lytic lesions
  2. Paraneoplastic (produces PTH related peptide)
  3. Increased conversion of inactive to active vitamin D
150
Q

How does PTH increase serum calcium

A

By activating bone resorption and increasing renal tubular resorption of calcium

Also increases activation of vitamin D which assists in increasing calcium resorption from the gut

151
Q

What does calcitonin do?

A

Produced by thyroid parafollicular C cells

Acts to reduce serum calcium through inhibiting bone resorption

152
Q

What is the definition of hypercalcemia

A

Corrected serum calcium of more than 2.6 mmol/L

*for every decrease of 10g/L in albumin, correct serum calcium by adding 0.2 mmol/L

153
Q

What are the mechanisms of hypercalcemia

A 
Increased bone destruction 
Decreased renal excretion 
Increased GI absorption 
Unregulated secretion of PTH 
Vitamin D abnormalities
154
Q

What causes primary hyperparathyroidism

A

Parathyroid adenoma
Parathyroid hyperplasia
Parathyroid carcinoma

155
Q

What ingested substances can cause hypercalcemia

A 
Increased vitamin d
Vitamin D intoxication 
Thiazide diuretics
Lithium intake 
Milk alkali syndrome
156
Q

What to ask on history for hypercalcemia

A 
Fatigue
Anorexia/weight loss 
GI complaints 
Bone pain
Tobacco use
Drug ingestion 
Excess vitamin ingestion
157
Q

What do you look for on physical exam for hypercalcemia

A

Usually unrevealing

Look for signs of malignancy (adenopathy, masses)

158
Q

What labs should you order in the hypercalcemia workup

A 
Intact PTH assay
Ionized Ca
Mg
Phosphate
ALP
Vitamin D
Lytes
Urea
Cr
If likely malignant-->
CXR
Urine for red cells (renal cancer)
Mammogram 
SPEP and UPEP
CT if no cancers yet found after above
159
Q

Symptoms of hypocalcemia

A 
Peri oral paresthesias
Tingling of fingers and toes
Tetany
Stridor (laryngospasm)
Seizures
Confusion
Weakness 
Meds (loop diuretics, bisphophonates, calcitonin, anticonvulsants)
160
Q

What changes might you see on ECG in hypocalcemia

A

Long QTc

ST changes

161
Q

How do you manage hypocalcemia

A

If severe symptoms–> CALCIUM GLUCONATE 1-2 amps slowly push IV then run calcium drip and MgSO4 drip over 4 hours

If mild symptoms–> calcium carbonate 1-2 g PO TID or QID with calcitriol PO

*treat underlying cause

162
Q

Causes of hypocalcemia

A
  1. PTH related–> low PTH, high phosphate
    - hypoparathyroidism (surgery, radiation, autoimmune, congenital, infiltrative)
    - functional hypoparathyroidism (hypomagnesemia)
  2. PTH resistance–> pseudo hypoparathyroidism
  3. Non PTH related
    - vitamin D abnormalities (will have high PTH) I.e nutritional, malabsorption, altered metabolism (cirrhosis, renal failure, anticonvulsants)
    - drugs (phosphate infusion causing hyperphosphatemia, calcitonin, loop diuretics)
    - hungry bone syndrome
    - acute–> acute pancreatitis, rhabdomyolysis, tumour lysis, toxic shock syndrome
    - other–> calcium malabsorption, hypoalbuminemia
163
Q

What organs are important in vitamin D metabolism/conversion?

A

Liver and kidney

164
Q

What does vitamin D do

A

Increases ca reabsorption in gut, kidney and bone
Increases phosphate reabsorption at gut and kidney
Decreases PTH

165
Q

What does PTH do?

A

Increases calcium reabsorption at distal tubule and bone
Decreases phosphate absorption at proximal tubule
Increases vitamin D

166
Q

What is the respiratory Ddx for dyspnea

A
  1. Airway–> COPDE, asthma exacerbation, acute bronchitis, infectious exacerbation of bronchiectasis, foreign body obstruction
  2. Parenchyma–> pneumonia, interstitial lung disease acute exacerbation, ARDS
  3. Vascular–> PE, pulm HTN
  4. Pleural–> pneumothorax, pleural effusion
167
Q

What is the cardiac Ddx for dyspnea?

A
  1. Myocardial–> HF exacerbation, MI
  2. Valvular–> Aortic stenosis, acute aortic regurgitation, mitral stenosis, endocarditis
  3. Pericardial–> pericardial effusion (tamponade)
  4. Vascular–> CAD (ACS, stable angina)
168
Q

What are the systemic Ddx for dyspnea

A

Anemia
Sepsis
Metabolic acidosis

169
Q

What are some non-cardiac/resp/systemic causes of dyspnea

A

Neuromuscular (can’t expand chest wall)
Psychogenic
Anxiety

170
Q

What causes of dyspnea present with:

  1. Sputum production
  2. Cough
  3. Pleuritic chest pain?
A
  1. Bronchitis, pneumonia, COPD
  2. Chronic bronchitis, asthma, pneumonia, airway irritation
  3. PE, spontaneous pneumothorax, pneumonia
171
Q

What causes of dyspnea present with:

  1. Visceral chest pain
  2. Hemoptysis
A
  1. Heart failure

2. PE, bronchitis, pneumonia

172
Q

What should you ask about on HPI for dyspnea?

A

Cough
Sputum production
Pleuritic or visceral chest pain
Hemoptysis
Risk factors–> smoking (COPD, bronchitis), cardiac Hx (HF), occupational or enviro exposures (asbestos, tire factory, dust)
Baseline fitness and change from baseline

173
Q

What causes of dyspnea may present with

  1. Wheeze
  2. Strider
  3. Consolidation/dullness to percussion
A
  1. Asthma, heart failure, COPD
  2. Upper airway obstruction
  3. Pneumonia
174
Q

What causes of dyspnea may present with

  1. Crackles/rales, S3, high JVP
  2. Cardiac murmur
  3. Tracheal shift from midline
A
  1. HF
  2. Valvular disease
  3. pneumothorax
175
Q

What causes of dyspnea may present with

  1. Leg swelling or pain
  2. Hyper expansion
  3. Fixed split S2, loud pulmonic component of S2, RV heave, JVP increased
A
  1. DVT–> PE
  2. COPD
  3. Pulm HTN
176
Q

What are signs of hyperexpansion seen in COPD?

A

Less than 4 cm tracheolaryngeal height
Barrel chest
Reduced cardiac dullness to percussion
Distant heart sounds

177
Q

What labs and investigations should be ordered in the setting of dyspnea?

A 
CBC, lytes, urea, Cr
Troponin
Calcium, magnesium, phosphate 
BNP if suspect HF
D dimer/CT PE if suspect PE
Sputum gram and culture
ECG (most common finding in PE is sinus tachy)
CXR--> pneumothorax, pneumonia (consolidation), HF (pleural effusions, Kerley B lines, batwinging, peri bronchial cuffing) 
Spirometry (FEV1/FVC)
ABG if in acute resp distress
Echo for valvular disease
178
Q

What tools can you use in assessing a possible COPDE

A

BODE index

GOLD classification

179
Q

What is the BODE index

A

BMI, Obstruction, Dyspnea, Exercise

Scoring system and capacity index used to test patients who have been diagnosed with COPD and predict long term outcomes for them

180
Q

What is the GOLD classification

A

Scoring system for COPD
Based on degree of airflow limitation measures with PFTs
Stages I–> IV are mild to severe

181
Q

What are COPDE triggers

A 
Infection 
Pollutants 
Non-adherence
PE
Pulmonary edema
Pneumothorax
COPD progression--natural course
182
Q

What is a normal FEV1/FVC?

A

70-85% (meaning most people blow out 70-85% of their inspiration in the first second of a forced vital capacity expiration)

183
Q

How does emphysema differ from the other lung diseases on PFTs

A

Increased TLC (same on everything else)

184
Q

How does interstitial lung disease differ from the other lung diseases on PFTs

A

Decreased residual volumes (the others have increased residual volume)

185
Q

How do you manage COPDE acutely?

A
  1. ABC–> keep O2 sat above 90% or between 88-92% if they are a CO2 retainer, establish IV access
  2. Bronchodilators–> salbutamol and ipratropium
  3. Steriods–> prednisone 40-60mg PO daily x 5-14 days (or methylprednisone IV)
  4. Abx–> give if any two of the following are present–> increased sputum prurulence, increased dyspnea or increased sputum volume –> consider lexofloxacin if no renal disease, doxycycline, amoxicillin, cefuroxime or azythromycin
  5. Consider need for BiPAP, intubation
    NPPV–> initiate early if mod/severe dyspnea, acidosis, increased PaCO2, RR higher than 25 as it results in 58% less intubation a and decreases length of stay and mortality
    Intubation if–> PaO2 less than 55-60 mmHg, increasing PaCO2, decreasing pH, increased RR, respiratory fatigue, change in mental status, or hemodynamics instability
  6. DVTP, chest physio
186
Q

How would you treat COPD long term?

A

Mild or moderate–> short acting inhaled bronchodilator PRN or standing inhaled bronchodilator (LAA better than LABA)

Severe or very severe–> inhaled corticosteroid + LAA and/or LABA

Smoking cessation in everyone 
Vaccinations in everyone 
Consider pulmonary rehab
Consider theophylline 
Home O2 as indicated
187
Q

Define hyperkalemia

A

K higher than 5 mmol/L

188
Q

Symptoms of hyperkalemia

A

Muscle weakness

Cardiac–> tall peaked T waves, wide QRS, wide and flat p wave, VF

189
Q

What are the causes of hyperkalemia?

A
  1. Pseudo hyperkalemia–> hemolysed blood sample, leukocytosis, thrombocytsis
  2. Increased intake –> rare
  3. Shift out of cells–> metabolic acidosis, diabetes (insulin deficit), beta blockade
  4. Increased release–> rhabdomyolysis, tumour lysis, strenuous exercise, intravascular hemorrhage
  5. Decreased output–> decreased distal renal tubular flow (renal failure, decreased effective circulating volume), hypoaldosteronism (decreased renin, adrenal insufficiency, renal tubular acidosis, ACEi, ARBs, spironolactone, NSAIDs)
190
Q

What labs would you order in a patient with hyperkalemia

A 
CBCD, lytes, urea, Cr, glucose
CK--rhabdomyolysis?
Serum osmolality
UA
Urine lytes
Urine osmolality

Calculate trans-tubular K gradient (TTKG)–> (Kurine x Osm-serum) / (Kserum x Osm-urine)

ECG
Hypoaldosteronism workup–> serum aldosterone and plasma renin activity
Rule out hemolysis and tumour lysis–> haptoglobin, LDH, peripheral smear, bili
Rule out shift–> acidemia
If GFR normal, consider decreased distal Na delivery and urine flow

191
Q

How do you treat hyperkalemia

A

Treat the underlying cause

In acute situations, must treat the hyperkalemia

more than 6.5 mmol/L is an emergency

  1. Stabilize membranes–> calcium gluconate
  2. Shift K+ into cells–> insulin (with glucose/D5), B agonists (albuterol), bicarbonate (exchanges K for H within cells)
  3. Promote K+ excretion–> diuretics to make them pee and kayexalate to make them poo it out
192
Q

Define hypokalemia

A

Less than 3.5mmol/L

193
Q

Differential for hypokalemia

A

Decreased intake

Increased shift of K into cells (beta agonism)

Increased losses

  • Renal–> diuretics, renal tubular defects, hyperaldosteronism (increased mineralocorticoids)
  • GI–> vomiting, NG suction, hypomagnesemia
194
Q

What are the symptoms of hypokalemia

A 
N/V
Ileus
Weakness
Muscle cramps
Rhabdomyolysis
Polyuria

Cardiac–> arrhythmia, sinus Brady or junctional tachy, AV block, VT, VF

ECG–> U waves, ventricular ectopic, ST depression, small T waves

195
Q

Investigations for hypokalemia

A 
CBC
Lytes
Urea
Mg 
Glucose
CK
Serum osmolality
UA
Urine lytes
Urine osmolality
196
Q

How do you manage hypokalemia

A
  1. Replace K-> KCl 10mEq in 100mL D5W bolus x3, continuous infusion max KCl concentration is 40mEq/L
  2. K supplement–> K-dur 20-120 mEq PO divided over once daily to QID–> oral preferred over IV in general
  3. Treat underlying cause

Internal Medicine General (4 decks)

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