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Internal Medicine General > Deck 3 > Flashcards

Deck 3 Flashcards

1
Q

What antibiotics cover anaerobes

A 
Clindamycin
Metronidazole 
Moxifloxacin 
Amox-clav
Pip-tazo 
Ertapenem
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2
Q

What antibiotics cover ESCAPPM bacteria

A 
Cipro
Gentamicin
Ceftazadime 
Cefepime 
Meropenem
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3
Q

What are the ESCAPPM organisms?

A 
Enterobacter 
Serratia 
Citrobacter 
Aeromonas 
Proteus 
Providencia 
Morganella
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4
Q

What antibiotics cover pseudomonas?>

A 
Cipro 
Gentamicin
Ceftazadime 
Cefepime 
Meropenem 
Pip-tazo
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5
Q

What antibiotics cover E. coli, klebsiella and proteus?

A 
Cipro
Gentamicin
Moxifloxacin 
Ceftriaxone 
Ceftazidime 
Cefepime 
Pip tazo
Amixicillin-->ecoli and klebsiella only 
Amox clav--> ecoli and klebsiella only 
Meropenem 
Ertapenem
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6
Q

What antibiotics cover strep?

A 
Penicillin
Amoxicillin 
Cephazolin
Clindamycin 
Vanco, linezolid 
Cipro 
Moxifloxacin 
Cefuroxime 
Ceftriaxone 
Cefepime 
Amox clav 
Pip tazo 
Meropenem
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7
Q

Which antibiotics cover MSSA?

A 
Cephazolin
Clindamycin 
Rifampin 
Vancomycin 
Linezolid 
Cipro 
Cefepime 
Amox clav 
Piptazo 
Meropenem
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8
Q

Which antibiotics cover MRSA

A 
Clindamycin 
Rifampicin 
Vancomycin 
Linezolid 
Daptomycin
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9
Q

What is typical angina

A

All three of–

  1. Substernal chest discomfort or heaviness
  2. Provoked by exertion or emotional stress
  3. Relieved by rest or nitro

(Atypical angina is two of the above)
(Non cardiac chest pain is none of the above)

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10
Q

What helps you call something “non cardiac” chest pain

A

None of the three features of typical angina

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11
Q

What are the CCS classes of angina?

A

I–chest pain with strenuous exercise
II–chest pain with more than two blocks flat ground or more than 1 flight of stairs
III–chest pain with 1-2 blocks flat ground or 1 flight of stairs
IV–chest pain at rest

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12
Q

What causes oxygen demand in the heart

A

HR
Contractility
Wall stress

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13
Q

What determines blood supply to the heart

A

Coronary vascular resistance
Oxygen carrying capacity
Coronary perfusion pressure

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14
Q

What are the 5 types of MI

A
  1. Type 1–spontaneous MI due to primary coronary event (atherosclerotic plaque rupture or erosion with acute embolic event)
  2. Type 2–MI secondary to ischemic imbalance (supply demand mismatch)
  3. Type 3–MI resulting in death when bio marker values are unavailable (sudden unexpected cardiac death before serum bio markers are collected for measurement)
  4. Type 4–MI related to PCI or stent thrombosis
  5. Type 5–MI related to CABG
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15
Q

What is an ACS

A

One of unstable angina, NSTEMI, STEMI

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16
Q

Define unstable angina

A

One of:

  1. Rest angina lasting more than 20 min
  2. New onset angina (angina CCS more than III within two months of initial presentation)
  3. Increasing angina (crescendo pattern–increased by at least one CCS class within two months of presentation to at least CCSIII)
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17
Q

Define NSTEMI

A

Any of the features of unstable angina with bio marker elevation (with or without ECG changes)

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18
Q

Define STEMI

A

Defined by ECG changes

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19
Q

What are the non modifiable cardiac risk factors

A

Age
Gender
Family history

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20
Q

What are the modifiable cardiac risk factors

A

Diabetes
HTN
Hyperlipidemia
Smoking

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21
Q

Which bio markers are the most specific in ACS?

A

CKMB and troponin but are typically not elevated until 4-8 hours after the injury and must be repeated at q6h initially

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22
Q

What are some other things other than ACS that can cause a rise in troponin

A

Demand ischemia–> sepsis, LVH
Myocardial ischemia–> coronary vasospasm, stroke
Direct myocardial damage–> cardiac contusion, chemo, pericarditis
Chronic renal insufficiency
Myocardial strain–> CHF, PE

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23
Q

What are the ST elevation cut offs in men and women? Where must these elevations be?

A

Must be in two contiguous leads

Greater than or equal to 0.2 mV for men and 0.15 mV for women in leads V2 and V3, otherwise greater than or equal to 0.1 mV in other leads

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24
Q

What are the non invasive cardiac imagining techniques

A

Echo
MIBI
Cardiac CT angio

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25
Q

What are the invasive cardiac imaging techniques

A

Angiography

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26
Q

What test should you do in a low risk UA/NSTEMI

A

Exercise MIBNI (examines perfusion)

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27
Q

What test should you do in a high risk UA/NSTEMI

A

Early catheterization

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28
Q

What should you do in a STEMI?

A

if in a PCI capable hospital–> catheterization ASAP

Non-PCI hospital–> skip imaging and go straight to fibrinolysis

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29
Q

What are the general treatment principles of an MI and how do you achieve them?

A
  1. Increase oxygen supply
    - -oxygen IF HYPOXIC
    - -nitrates, morphine (vasodilation)
    - -anti platelets–> ASA, plavix or alternative
    - -anti coagulation–> heparin
    - -relieve obstruction–> PCI, CABG, thrombolytics
  2. Decrease demand
    - -treat underlying cause of the increased demand (I.e sepsis)
    - -beta blockers
  3. Secondary prevention and myocardial recovery
    - -statins
    - -ACEi
    - -MRAs
    - -lifestyle
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30
Q

What is the treatment specifically for STEMI?

A
  1. Anti thrombotic therapy–> ASA, clopidogrel or ticagrelor, heparin or enoxaparin
  2. Reperfusion therapy–> PCI, thrombolytics (if STEMI), CABG if indicated
  3. Ancillary therapy–> nitro (anti angina), beta blocker, ACEi, MRA, statin, secondary prevention
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31
Q

What are the absolute contraindications to thrombolysis

A
  1. History of intracranial hemorrhage
  2. Ischemic stroke in the past 3 months
  3. Cerebral malformation or tumour
  4. Possible aortic dissection
  5. Bleeding diathesis
  6. Significant head trauma in past 3 months
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32
Q

What are some of the relative contraindications to thrombolysis

A 
Poorly controlled BP
Ischemic stroke more than 3 months ago
Dementia
Traumatic prolonged CPR
Major surgery in past three weeks
Internal bleeding in past four weeks
No compressible vascular punctures
Pregnancy
Warfarin
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33
Q

What 4 meds should someone who suffered an ACS be discharged on and why

A
  1. ASA
  2. Beta blocker
  3. ACEi
  4. Statins
    ..each Med decreases future events by 25% (relative risk reduction) so best to be on all 4

Also..
Dual anti platelet therapy for more than 1 months for a bare metal stent, 1 year for a drug eluding stent and 1 year following ACS

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34
Q

What is the definition of thrombocytopenia

A

Normal platelets –> 150-400 (000) per mcl of blood

Thrombocytopenia is less than 150

a drop of more than 50% warrants investigation

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35
Q

What are the consequences of the following platelet levels

  1. Less than 50
  2. Less than 20
  3. Less than 10
A
  1. Surgical bleeding (100 for neuro surg)
  2. Risk of severe bleed with fever
  3. Risk of spontaneous bleeding (always look for neuro symptoms, need to rule out an intracranial bleed in these people when they present)
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36
Q

What is the overall approach to a thrombocytopenia?

A
  1. Increased destruction
  2. Decreased production
  3. Sequestration
  4. Other
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37
Q

What causes of thrombocytopenia fall under the “increased destruction” category?

A
  1. Non immune–>
    MAHAs
    Infection
    Meds and toxins
  2. Autoimmune–>
    Immune thrombocytopenic purpura (ITP)
    Heparin indicted thrombocytopenia
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38
Q

Name the MAHAs

A

Thrombotic thrombocytopenic purpura (TTP)
Hemolytic uremic syndrome (HUS)
Disseminated intravascular coagulation (DIC)
HELLP syndrome
Vasculitis and scleroderma crisis
Hypertensive crisis
Mechanical (mechanical heart valves etc)

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39
Q

Name the autoimmune causes of increased platelet destruction

A

ITP

HIT

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40
Q

What are the three categories of decreased production of platelets causing thrombocytopenia

A
  1. Hypo cellular
  2. Hyper cellular
  3. Bone marrow replacement or infiltration
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41
Q

What are the hypo cellular causes of decreased platelet production

A 
Aplastic anemia
Meds, toxins, substances 
Infection (sepsis, viral I.e HIV, parvovirus etc)
Vitamin B12 and folate deficiency 
Liver cirrhosis 
Autoimmune disorders
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42
Q

What are the hyper cellular causes of decreased platelet production

A

MDS
Leukaemia and lymphoma
Multiple myeloma
HLH

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43
Q

What are the bone marrow replacement/infiltration causes of reduced platelet production

A

Myelofibrosis
Granulomas (TB, fungal, sarcoidosis)
Solid organ malignancies (mets breast, prostate, liver)
Haematological malignancies

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44
Q

What causes increased sequestration of platelets

A

Splenic pooling due to spenomegaly (I.e portal HTN)

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45
Q

What are the “other” causes of thrombocytopenia

A

Psueothrombocytopenia–> platelets clump in tube

Dilutional thrombocytopenia –> post transfusion of a large volume of pRBCs (usually more than 10 units)

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46
Q

What causes TTP?

A

Decreased ADAMTS13 protease activity–> can’t cleave the huge VWF multiverse on endothelial cell surface–> platelets stick to the endothelial surface–> huge clumps of platelets–> messes up the RBCs coming through–> SCHISTOCYTES and consumptive thrombocytopenia but NO activation of coagulation cascade (therefore coags normal)

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47
Q

What is the clinical Pentad of TTP and how many do you need for a diagnosis

A 
Need 2 of--
Thrombocytopenia
MAHA
Renal failure
Fever
Mental status changes
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48
Q

What are some conditions associated with TTP

A 
Infection--HIV, ecoli 
Autoimmune conditions
Pregnancy
Malignancy 
Drugs (rare)
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49
Q

What is the treatment for TTP

A

Aspirin
Steroids
FFP–> this has ADAMTS13 in it so it can go around cleaving the big VWF clumps

Definitive therapy is PLEX (plasma exchange)

TTP is a medical emergency and mortality without treatment is about 90% (with tx is 20)

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50
Q

What is the classic triad of HUS

A

MAHA
Thrombocytopenia
Acute renal failure

**associated with shiga toxin produced by ecoli

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51
Q

What is the precipitating factor in DIC

A

Activation of the coagulation cascade –> leads to thrombosis in the micro vasculature

  • -> ischemia of end organs–> multi organ failure
  • -> MAHA–> SCHISTOCYTES
  • -> consumption of platelets AND FACTORS–> tcp AND COAGULOPATHY –> both clots and bleeding
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52
Q

What precipitates DIC

A 
Trauma
Infection
Malignancy
Obstetrical complications 
Toxins (snake bites)
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53
Q

Describe acute DIC

A

Severe coagulopathy with diffuse bleeding, ARF, hepatic dysfunction, ARDS

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54
Q

Describe chronic DIC

A

Milder bleeding

Arterial and venous thrombosis with malignancy

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55
Q

How can you differentiate DIC from TTP

A

Both have low platelets and large platelets and schistocytes on smear

TTP–> many schistocytes on smear, normal fibrinogen, normal INR/PTT

DIC–> fewer schistocytes on smear, low fibrinogen and high INR/PTT

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56
Q

What is primary ITP?

A

Can’t ID underlying cause

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57
Q

What is secondary ITP

A

Caused by
Drugs (I.e heparin)
Infections (HIV, EBV, CMV, HCV, H pylori)
Malignancy (CLL, lymphoma)
Autoimmune (SLE, anti phospholipid antibody syndrome)
Alloimmune (post transfusion)

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58
Q

What is the only cause of single digit platelets that you will likely see?

A

ITP

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59
Q

What are the symptoms of ITP

A

Petechiae
Purpura
Easy bruising

Usually very low platelet count, always less than 100 often less than 10

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60
Q

What is the most common (perhaps only) cause of isolated thrombocytopenia (no other cell lines affected at all)

A

ITP

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61
Q

How do you diagnose ITP

A

Isolated thrombocytopenia
VERY low platelets
Large platelets on peripheral smear
*diagnosis of exclusion

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62
Q

What must you rule out before dx of ITP

A

MAHA

Secondary causes

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63
Q

How’d you treat ITP

A 
Prednisone--works in 1-2 weeks
IVIG--works in 1-2 days
Rhogam (for Rh+ pts)
New TPO agonists 
Rituximab
Splenectomy
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64
Q

What is HIT?

A

HIT type 1–mild tcp within the first two days of starting heparin, counts return to normal while the patient is still on heparin (due to platelet clumping)

HIT type 2–5-10 days post starting heparin, more serious form caused by antibodies targeting heparin and PF4 complex on platelets–> high risk of thrombotic complications (DVT, PE)
–will likely see lesions at puncture site

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65
Q

What is the treatment for HIT

A

Stop heparin
Start alternative anticoagulant–> argatroban, fondaparinux are not approved for use in HITT but are often used due to expert consensus
DO NOT start warfarin until substantial platelet recovery

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66
Q

What should you ask on history of tcp?

A
  1. Timing of platelet count drop and other cell lines involved
  2. Decrease production–>
    - -recent infection (BM suppression? Secondary ITP?)
    - -history of autoimmune diseases
    - -detailed Med history
    - -EtOH intake, nutritional status
    - -history of liver disease
    - -history of constitutional symptoms, malignancies, malignancy screening
    - -history of granulomatous disorders, TB exposure
  3. Increased destruction–>
    - -history of HIV, HBV, HCV
    - -history of h pylori
    - -history of heparin exposure
    - -history of DIC triggers
    - -history of pregnancy, meds, autoimmune disease (TTP triggers)
    - -history of diarrhea (?HUS)
  4. Abdo pain/distension or early satiety for splenomegaly
  5. Consequences of the top–>
    - -mucocutaneous bleeding (nose, gingiva, GI, easy bruising)
    - -neuro symptoms (ICH)
    - -history of bleeding with surgery, childbirth, dental work
    - -transfusion history
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67
Q

What should you look for on exam for tcp?

A

General

H&N–> orzo pharyngeal petechiae, SLE rash, alopecia, pupils

CVS–> murmur (MAHA)

Abdo–> splenomegaly, tenderness, findings of chronic liver disease

Derm–> bruising, petechiae, bleeding skin, rashes

MSK–> joint effusions, thrombosis

Neuro–> CN II-XII, gross sensory and motor (ICH)

Lymph nodes–> H&N, axillary, inguinal

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68
Q

What labs would you order to investigate the following causes of tcp–

  1. MAHAs (HUS/TTP/DIC) overall
  2. DIC
  3. HUS/TTP
A
  1. Total/direct bilirubin, LDH, haptoglobin, peripheral smear (schistocytes), BUN and Cr (ARF)
  2. INR, PTT, D-dimer, fibrinogen level
  3. 5 Cardinal features, peripheral smear
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69
Q

What labs would you order to investigate the following causes of tcp–

  1. HIT
  2. ITP
A
  1. Calculate 4T score

2. Large platelets, isolated tcp

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70
Q

What labs would you order to investigate the following causes of tcp–

  1. Infection
  2. Malignancy
  3. Autoimmune
A
  1. HIV and hepatitis serology, urea breath test
  2. Peripheral smear, LDH, SPEP, age appropriate screening
  3. If suggested by clinical features, order ANA
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71
Q

What labs would you order to investigate the following causes of tcp–

  1. Bone marrow disease
  2. Liver disease (malignancy)
  3. Hypersplenism
A
  1. SPEP/UPEP, calcium, retics, B12, MCV, blast forms (leukaemia), teardrop (myelofibrosis), BM biopsy if still on Ddx (older patient, B sx, no other cause)
  2. LFTs and liver enzymes
  3. Physical exam or abdo U/S
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72
Q

Ddx peri umbilical or diffuse abdo pain

A

AAA

Ischemic bowel (secondary to underlying atherosclerotic disease or arterial embolism from Afib or valvular disease)

Bowel obstruction

Pancreatitis

Gastroenteritis

Metabolic disturbances

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73
Q

Ddx RUQ pain

A

Cholescystitis

Biliary colic

Hepatitis

Pyelonephritis

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74
Q

Ddx RLQ pain

A

Appendicitis

Nephrolithiasis

Crohn’s disease

Ovarian cyst or torsion

Ectopic pregnancy

PID

Testicular torsion

Inguinal herniation

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75
Q

DDx LUQ pain

A

Splenic rupture or infarct

Pyelonephritis

LLL pneumonia

Pancreatitis

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76
Q

DDx LLQ pain

A

Diverticulitis

Nephrolithiasis

IBD

Ovarian cyst/torsion

Hernia

Testicular torsion

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77
Q

What should you ask on history for abdo pain?

A

Changes with food?
Changes with position?
Fevers, chills, sweats?
N/V/D?

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78
Q

What would you expect on history for PUD

A

Pain diminishes with meal, gets worse after fatty meals

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79
Q

What would you expect on Hx and imaging for perforated viscus??

A

Sudden onset

Air under diaphragm on plain film

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80
Q

What would you expect on history for peritoneal irritation

A

Moving slowly, hunching forward to avoid jarring

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81
Q

What would you expect on Hx, physical for appendicitis? How to dx?

A

Starts vague, cramp like abdo pain that moves to RLQ and becomes sharper and more intense

Rebound tenderness, pain at mcburney’s, rovsings, obturator

Dx with CT

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82
Q

What would you expect on Hx and physical for diverticulitis

A

LLQ pain

Rebound tenderness

Dx with CT

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83
Q

What would you expect on history for biliary colic? What test would you order?

A

Severe, aching, steady pain in RUQ or epigastrium, lasts 1-4 hours, may be associated with meal

Amylase–> mild increase

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84
Q

What would you expect on history, physical for cholescystitis? What would you order for tests and imaging?

A

Persistent pain associated with fever and may radiate to R scapula

Murphys sign positive

Include ALP/GGT/Bili (cholestatic picture is increased bili and ALP)

On US–> thickened gallbladder, sonographic murphys, pericholecystic fluid

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85
Q

What would you expect on history, physical for pancreatitis? Workup?

A

Epigastric/peri umbilical pain, radiates to back, relieved with sitting, Hx of recent alcohol use

++ pain in RLQ, bowel sounds absent

Lipase

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86
Q

What would you expect on history, physical for ischemic bowel? Workup?

A

Sudden and severe onset
Hx Afib

Lots of pain in epigastrium and peri umbilical areas
Bowel sounds absent

Include lactate, lytes, amylase
Do CT

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87
Q

What would you expect on Hx for bowel obstruction?

A 
Cramps mid abdominal pain 
Paroxysms 
History of abdo surgery
Absence of recent BMs
Absence of flatus
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88
Q

What would you expect on history for nephrolithiasis?

A

Begins gradually then escalates to severe pain in 20-60 min with flank pain radiating to groin or testicle

Hematuria on UA

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89
Q

What would you expect on history for AAA? On exam?

A

Pain radiates to back
History of vascular disease

Palpable, pulsating mass with diminished peripheral pulses

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90
Q

What would you expect on history, physical and labs for liver disease/hepatitis?

A

RUQ pain

Jaundice

Marked increase in LFTs, transaminitis (AST, ALT)

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91
Q

What would you expect on history and exam for gastroenteritis? What do you do?

A

N/V/D

Usually benign, diffuse tenderness

Observation, resuscitation with fluids as necessary

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92
Q

What would you expect on history and workup for DKA?

A

Abdo pain, nausea, vomit

Ketouria
Anion gap acidosis

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93
Q

What is a mnemonic for the causes of diarrhea?

A

MISO

Motility
Inflammatory (bloody)
Secretory
Osmotic

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94
Q

What are the Motility causes of diarrhea

A 
Hyperthyroid
Diabetic neuropathy
Bacterial overgrowth 
IBS
Scleroderma
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95
Q

What are the inflammatory causes of diarrhea

A
  1. Infections (invasive)–> salmonella, shigella, campylobacter, EHEC, EIEC, C diff, vibrio, yersinia
  2. Inflammatory–> UC, Crohn’s, ischemia, radiation, toxic
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96
Q

What are the secretory causes of diarrhea

A
  1. Infections (non invasive)–> viral (rotavirus, norovirus), vibrio, cholera, staph, b cereus, ETEC, EPEC, giardia, cryptococcus, amoeba
  2. Neuro endocrine–> carcinoid tumours, VIPoma, calcitonin excess, gastrinoma
  3. Meds–> laxatives, PPIs
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97
Q

What are the osmotic causes of diarrhea

A
  1. Maldigestion or malabsorption –> pancreatic insufficiency, celiac disease, lactose intolerance
  2. Medications–> antacids, antibiotics, Mg, lactose, sorbitol, colchicine, metformin
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98
Q

What should you ask on a history of diarrhea

A

Characterize onset, duration, frequency, volume, floating

Bloody versus non bloody

Abdo pain or weight loss

Sick contacts, travel, food, Med changes, swimming, camping

PMHx of DM, hyperthyroid, IBS, lactose intolerance, bowel surgery

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99
Q

What should you look for on physical exam of patient with diarrhea

A 
Vitals
Volume status
Body weight
Abdo tenderness
Rectal exam for FOB
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100
Q

What labs would you order in a patient with diarrhea

A

CBCD, lytes, urea, Cr, lactate
–> if chronic diarrhea, add TSH, anti TTG antibody (celiac) + IgA level, andomysial antibody

Stool sample for C&S, O&P, c diff toxin, viral culture

Fecal osmotic gap

Fecal testing for giardia toxin

CTabdo if indicated

Endoscopy

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101
Q

How do you treat diarrhea

A

Depends on the cause
Symptom control with IV fluids
Anti diarrheals if not inflammatory diarrhea–> loperamide

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102
Q

How do you treat shigella, campylobacter, ecoli diarrhea

A

Levofloxacin

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103
Q

How do you treat vibrio cholera diarrhea

A

Tetracycline or doxycycline

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104
Q

How do you treat cyclospora diarrhea

A

Septra

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105
Q

How do you treat c diff, giardia, entamoeba diarrhea

A

Metronidazole

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106
Q

What are the SECSY bacteria

A 
Shigella
Ecoli 
Campylobacter 
Salmonella 
Yersinia

+c diff, entamoeba histolytica

INVASIVE INFECTIOUS

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107
Q

How do you treat infections with the SECSY bacteria?

A

Cipro

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108
Q

How do you treat IBD

A

5-ASA, corticosteroids, immunosuppressants

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109
Q

Ddx of neutrophilia (left shift)

A
  1. Infection–> usually bacterial
  2. Inflammation–> MI, PE, burns
  3. Neoplasm–> myeloproliferative neoplasm
  4. Drugs and toxins–> corticosteroids, beta agonists
  5. Stress–> release of endogenous corticosteroids and catecholamines
  6. Marrow stimulation–> hemolytic anemia, ITP
  7. Asplenia–> surgical, SCD
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110
Q

Ddx lymphocytosis

A
  1. Infection–> usually VIRAL
  2. Autoimmune–> RA
  3. Neoplasm–> leukaemia (CLL), lymphoma
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111
Q

Ddx monocytosis

A
  1. Infection–> TB, listeria, rickettsia, fungi, parasites
  2. Inflammation–> IBD, sarcoidosis, collagen vascular disease
  3. Neoplasm–> Hodgkin lymphoma, leukaemia
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112
Q

Ddx eosinophilia

A
  1. Infection–> usually parasitic
  2. Allergic–> drugs, asthma, eczema
  3. Neoplasm–> Hodgkin lymphoma, CML
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113
Q

Ddx basophilia

A
  1. Neoplasm–> MPN, HL

2. Inflammatory/allergy–> IBD, chronic airway inflammation

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114
Q

What should you ask on history in a leukocytosis?

A

Infection–> fever, chills, sx of infective focus

Cancer–> night sweats, weight loss, thrombocytopenia/anemia

Autoimmune–> joint pain, diarrhea, abdo pain, signs of SLE

Meds, allergies, possible exposures

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115
Q

Investigations for a leukocytosis

A 
CBCD
Peripheral smear
Lytes
BUN
Cr
Glucose

If suspect mi–> troponin, ECG

Pan cultures

Autoimmune workup–> ANA, RF, ANCA

Imaging–> CXR, CT, PET, US lymph nodes, echo

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116
Q

Viral causes lymphadenopathy

A 
HIV
EBV
CMV
HSV
VZV
Hepatitis
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117
Q

Bacterial causes of LAD

A

Generalized–> TB, syphilis

Localized–> staph, strep, cat scratch

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118
Q

Fungal/parasitic causes of LAD

A

Histoplasmosis

Toxoplasmosis

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119
Q

Immune related causes of LAD

A

Autoimmune–SLE, RA, scleroderma

Serum sickness

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120
Q

Neoplastic nausea of LAD

A

Lymphoma
Leukaemia
Metastatic CA

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121
Q

Infiltrative causes of LAD

A

Sarcoidosis

Amyloidosis

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122
Q

What to ask on Hx in LAD

A 
Infective ROS
Malignancy ROS
Hx autoimmune disease--joint swelling, SLE sx
Risks for HIV, hepatitis etc
Pancytopenia
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123
Q

What factors favour doing a lymph node biopsy in the setting of LAD

A

Older than 40
LN bigger than 2cm
Greater than 1 mo duration

ALWAYS biopsy a supraclavicular LN as it is always abnormal

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124
Q

Name the primary epilepsies

A

Partial (simple, complex, secondarily generalized)

Generalized (absence, generalized tonic-clinic, myoclonic, atonic, tonic, clonic)

Unknown (epileptic spasms)

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125
Q

Name the structural causes of unprovoked epileptic seizures

A

Stroke (infarction)

Head trauma

Brain tumours

Neuro-degenerative disorders

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126
Q

Name the infectious causes of unprovoked epileptic seizures

A

Encephalitis

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127
Q

Name the congenital causes of unprovoked epileptic seizures

A

Neuronal migration errors and cortical dysgenesis

Vascular malformations

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128
Q

Name drugs that lower the seizure threshold

A

Bupropion

Theophylline

Isoniazid

Imipenem

High dose penicillin

Meperidine

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129
Q

Withdrawal from what substances can cause provoked seizures?

A

Alcohol

Benzodiazepines

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130
Q

Overdoses on what substances can cause provoked seizures?

A

Methanol

Ethylene glycol

TCAs

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131
Q

Which illicit drugs can cause provoked seizures (even if not OD)?

A

Cocaine

Amphetamines

LSD

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132
Q

Name the metabolic causes of (provoked) seizures

A

Hypoglycaemia

Non ketotic hyperglycaemia

Hyponatremia

Hypocalcemia

Uremia

Hypoxia (cerebral anoxia)

Hyperthyroidism

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133
Q

Infectious causes of provoked seizures

A

Meningitis

HSV encephalitis

Febrile seizures

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134
Q

What relatively common heart condition can cause provoked seizures

A

Arrhythmias

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135
Q

What conditions can mimic seizures

A 
Syncope
TIA
Migraine 
BBPV
Hypoglycaemia 
Sleep disorders (narcolepsy, OSA)
Periodic paralysis
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136
Q

What is the pathophysiology of generalized seizures

A

Engages the cortex bilaterally, with loss of consciousness

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137
Q

What is the pathophysiology behind focal seizures without impairment of consciousness or awareness

A

Originate in one hemisphere

Possible motor, sensory, autonomic or psychic symptoms with sparing of consciousness and awareness

Used to be known as “simple partial seizure”

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138
Q

What is the pathophysiology behind focal dyscognitive seizures

A

Originate in one hemisphere

Possible motor, sensory, autonomic, psychic symptoms with IMPAIRED consciousness or awareness

Used to be known as a “complex partial seizure”

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139
Q

What is the pathophysiology behind a focal evolving to bilateral convulsive seizures

A

Originates in one hemisphere but evolves to engage the cortex bilaterally

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140
Q

What does a clonic seizure look like

A

Jerky contractions, rhythmic

141
Q

What does a tonic seizure look like

A

Muscle stiffening

142
Q

What is the definition of epilepsy

A

Any one of the following 3 criteria:

  1. 2 or more unprovoked seizures more than 24 hours apart
  2. 1 unprovoked seizure with probability of another seizure more than 60% over the next 10 years (i.e presence of a structural lesion associated with high risk for seizure recurrence)
  3. Diagnosis of epilepsy syndrome
143
Q

What is status epilepticus

A

5 or more minutes of continuous seizure activity or more than two discrete seizures without complete recovery of consciousness in between events

144
Q

What are some complications that can arise due to seizures

A 
Seizure related injuries
Aspiration pneumonia 
Neurogenic pulmonary edema 
Hypoxic brain injury 
Cardiac injury 
Rhabdomyolysis (leading to acute renal failure and hyperkalemia)
Lactic acidosis 
Sudden unexpected death in epilepsy (SUDEP)
145
Q

What should you ask on history for a seizure

A

When was the first seizure

Prodrome

Aura

Ictal symptoms

Post ictal period

Diurnal variation

History suggestive of missed seizure (I.e waking up with sore muscles, blood in mouth or urinary incontinence)

Precipitants (sleep deprivation, skipped meals, stress, messes, alcohol, missed medications, medication withdrawal)

Maximum seizure free period

Seizure types

Related injuries

Driving

Employment

146
Q

What labs would you order to work up a seizure

A 
CBCD, lytes, urea, Cr, glucose
Ca, Mg, PO4
Liver enzymes, bilirubin, albumin
CK, troponin
TSH
INR, PTT

**PROLACTIN–> acute increase in 10-20 min after generalized tonic clonic seizure, low sensitivity

147
Q

What imaging would you order in the setting of a seizure

A

CT head

MRI

148
Q

What other tests might you order to workup a seizure

A

EEG with or without sleep deprivation

Order for unprovoked or recurrent seizures (best done within 24 hours of seizure onset)
Consider sleep deprived EEG to increase yield of detecting epileptiform activity/focal abnormality

–Also, CXR if suspect aspiration and LP if suspect meningitis or encephalitis as a cause of the seizure

149
Q

What is an aura

A

Focal seizure with subjective sensory or psychic phenomenon

150
Q

What is a Jacksonian March

A

Focal motor seizure of primary motor cortex which produces clonic activity in the contra lateral side of the body

Rhythmic activity spreads to adjacent areas (I.e fingers to wrist to arms)

151
Q

What is Todd’s paralysis

A

Hemiparesis or hemiplegia following a seizure, which suggest focal onset

152
Q

What can EEG be used to diagnose

A

Useful for epilepsy (40-50% sensitivity, high specificity)

Metabolic and toxic encephalopathies

Herpes encephalitis

Subacute sclerosing panencephalitis

Prion diseases

153
Q

How do you manage status epilepticus

A

ABC
Oxygen
IV access
STAT investigations (ABG, CBCD, lytes, Cr, glucose, Mg, Ca, PO4, toxic screen, anti epileptic drug level)
Glucose if hypoglycaemic –> thiamine in 50% dextrose IV

FIRST LINE–> lorazepam IV
Second line–> phenytoin IV
Third line–> midazolam
Fourth line–> anesthetic doses of propofol IV, need to intubate

**phenytoin and benzodiazepines are incompatible with same IV use, will precipitate if used in same line; use separate IV sites

154
Q

What do you use for acute seizure control

A 
Benzodiazepines (lorazepam IV)
Anti epileptic (phenytoin... Or phenobarbital, carbamazepine, valproate)

IF EtOH WITHDRAWAL–> add thiamine

*do not use same IV for benzodiazepines and phenytoin

155
Q

How do you manage seizures long term

A

Valproic acid–titration up to typical daily dose of 750-2000 mg PO daily
–most effective

Lamotrigine–titration up to typical daily dose of 100-400 mg

Topiramate–titration up to typical daily dose of 200-400 mg

Keppra

Carbamazepine

Gabapentin

156
Q

What ministry do you need to check with if you have a patient with seizures

A

Motor vehicles–may have to report

157
Q

Do you start anti seizure medications in a first time seizure?

A

If there is no structural lesion, no physical findings, and normal EEG, usually do not need to start antiseizure medications

Risk of recurrence after first seizure is 30-60%

Risk after second seizure is 80-90%

158
Q

When may you consider stopping epileptic meds

A

After a seizure free period of 2-5 years

159
Q

What are the top 5 drug induced seizure etiologies

A

Isoniazid–treat with pyridoxine

Theophylline–>supportive tx

Oral hypoglycemic agents–treat with glucose with or without octreotide and glucagon

Carbon monoxide–supportive tx and oxygen

Bupropion–supportive tx

160
Q

Define Alzheimer’s

A

General sequence of changes include mood alterations, and slow, progressive cognitive decline

Primarily affects memory, language and visuospatial domains early on
Early motor symptoms are rare but may have apraxia later

Loss of functional autonomy, neuropsychiatric manifestations, Parkinsonism may be seen I more advanced stages of disease

CT may show white matter change

Mostly a diagnosis of exclusion but accounts for about 60% of dementia so

161
Q

Define vascular dementia

A

Acute STEPWISE or slow progressive decline

May have focal neurological deficits

MMSE patchy

CT may show white matter change

Pure vascular dementia is uncommon, more frequently occurs along with Alzheimer’s like dementia (mixed vascular)

162
Q

Define Parkinson’s dementia

A

Parkinson’s disease diagnosed for more than a year prior to cognitive onset

Slow decline

Parkinson’s patients have 6x increased risk of dementia

163
Q

Define Lewy body dementia

A

Progressive memory decline

Parkinsonism

Visual hallucinations

Fluctuating cognition (especially attention/alertness)

Visuospatial domain often markedly impaired

Supportive features–> adverse hypersensitivity to typical antipsychotic meds, syncope, falls, delusions, sleep disturbance

164
Q

Define frontotemporal dementia

A

Age usually less than 60

Behavioural symptoms noticeable before cognitive impairment–> disinhibited or passive presentation, impaired judgment, significant social indifference, declining hygiene, prominent language deficits but amnesia less noticeable early on

Early primitive reflexes/incontinence

Late akinesia, rigidity, tremor

Impaired executive function

**MMSE may be normal

CT shows FRONTO TEMPORAL ATROPHY

165
Q

What are the potentially reversible causes of dementia

A
  1. Metabolic–> alcoholism, vitamin B12 deficiency, hypothyroidism
  2. Structural–> normal pressure hydrocephalus (NPH), subdural hemorrhage, neoplastic, vascular
  3. Infectious–> chronic meningitis, HIV, neurosyphilis, Whipple’s
  4. Inflammatory–> vasculitis, hashimotos encephalitis, MS
166
Q

What conditions does dementia mimic?

A

Depression
Delirium
Developmental disorders
Age associated memory impairment

167
Q

What physical findings might you expect to find in

  1. Alzheimer’s
  2. Vascular
  3. Fronto temporal
A
  1. Relatively normal
  2. Focal neuro deficits
  3. Primitive reflexes, disinhibited or passive
168
Q

What MMSE findings might you expect to find in

  1. Alzheimer’s
  2. Vascular
  3. Fronto temporal
A
  1. Memory recall affected early on, then language and visuospatial deficits
  2. Patchy changes
  3. May be normal
169
Q

What changes might you see on CT head in

  1. Alzheimer’s
  2. Vascular
  3. Fronto temporal
A
  1. White matter changes
  2. White matter changes
  3. Frontotemporal atrophy
170
Q

What labs might you order to work up dementia

A

CBCD, lytes, creatinine, glucose, calcium, TSH, vitamin B12

Imaging CT head

Could also do:
AST, ALT, ALP, bilirubin, RBC folate, VDRL, HIV serology, urine collection for heavy metals

171
Q

What are the DSM V criteria for a major neuro cognitive disorder

A
  1. A decline in one or more than one cognitive domain–> learning and memory, language, executive function, complex attention, perceptual abnormalities, social cognition
  2. Cognitive deficits must impair at least one IADL
  3. Cognitive deficits do not occur during delirium and are not better explained by another psychiatric disorder
172
Q

What is the Hachinski Ischemic Score

A

A scoring system used to help distinguish between Alzheimer’s and vascular dementia

Includes points like fluctuating course, depression, stepwise progression etc

Score of less than 4 suggests Alzheimer’s is likely

A score of more than 7 suggests likely vascular dementia

173
Q

What does an abnormal clock drawing test suggest

A

Dementia

LR +5.3

(Normal clock drawing is not useful as half of demented patients can produce a normal clock)

174
Q

What are the criteria for ordering a CT head in a dementia patient

A

Age less than 60
Rapid onset of 1-2 months
Unexplained decline in cognition or function
Dementia of short duration–less than two years
Unexplained neuro symptoms
Early incontinence or gait problems (NPH)
Recent head trauma
History of cancer or bleeding disorder
New localized signs

175
Q

Management of dementia–what are the different aspects to consider?

A
  1. Risk reduction
  2. Disease management
  3. Symptoms management
  4. Tube feeing
176
Q

What can be done for risk reduction in dementia

A

Anti hypertensive

Dyslipidemia treatment

177
Q

What can be done for disease management for dementia

A

Start an anticholinesterase for Alzheimer’s (donepizil, rivastigmine_
–avoid if has seizures, cardiac conduction problems, significant asthma, COPD or recent GI bleed

Memantine may be used as a single agent or as add on therapy to above

178
Q

What can be done for symptom management in dementia

A

Treat problem behaviours with non pharmacological and pharmacological approaches ( trazodone, atypicla antipsychotics)

Treat co existing depression

179
Q

Is tube feeding recommended in dementia?

A

Generally not in advanced dementia due to increased risk of complications without evidence of clinical benefit (I.e no increase in survival or quality of like or prevention of aspiration pneumonia_

180
Q

What causes normal pressure hydrocephalus (NPH)

A

Inflammation and fibrosis of the arachnoid granulations–> decreased absorption of CSF–> hydrocephalus–> normal opening pressure but elevated pressure over peri ventricular white matter tracts

Idiopathic or secondary to subarachnoid hemorrhage, chronic meningitis etc

181
Q

How does NPH present?

A

Classic triad of gait apraxia (magnetic gait as feel are stuck to floor), urge incontinence, cognitive decline

May also have postural instability, lower extremity spasticity, hyperreflexia, extensor plantar responses

182
Q

How do you diagnose NPH

A

Clinically and with MRI

Improvement of gait or cognition 1 hour after removal of CSF helpful for diagnosis (Fisher test, PPV of 90-100%)

183
Q

Treatment for NPH

A

LP, shunts

184
Q

What are the Parkinson’s plus syndromes?

A

Progressive supra nuclear palsy

Etc…

185
Q

How does CJD present?

A

Rapid progression, characteristic EEG, myoclonic jerks, expected death within 6-12 months

186
Q

How does huntington’s dementia present?

A

Autosomal dominant with incomplete penetrance

187
Q

What is the mnemonic for decreased LOC/delirium?

A 
DIMS
Drugs
Infection 
Metabolic
Structural 
(R--retention)
188
Q

What is the mnemonic for the drug causes of delirium?

A

ABCD

Alcohol (intoxication and withdrawal)
anticholinergics (atropine, benztropine)
antidepressants (SSRIs, TCAs)
analgesics (opioids, NSAIDs, steroids)
antibiotics (penicillins, quinolones, isoniazid, rifampin)
Antihistamines (cimetidine, ranitidine)

Benzodiazepines and barbiturates (intoxication and withdrawal)

Cardiac (amiodarone, beta blockers, digoxin, diuretics)
Dopamine agents (amantadine, bromocriptine, levodopa)
189
Q

What are the metabolic causes of delirium

A

Organ failure–> hepatic, anorexia, hypothyroidism, thyrotoxicosis, hypoxia, hypercapnea, hypothermia, hypertensive

Electrolyte imbalance–> ketoacidosis, hyper or hypoglycemia, hyponatremia, hypernatremia, hypomagnesemia, hypercalcemia

190
Q

What are the structural causes of delirium

A
  1. Hemorrhage–> subarachnoid, epidural, subdural, intracerebral
  2. Stroke–> basilar
  3. Tumour
  4. Abscess
191
Q

Why is delirium so common in the hospitalized elderly?

A

Limited reserve so easy to tip over into delirium

192
Q

What are the subtypes of delirium

A
  1. Hyperactive delirium–> characterized by agitation and/or hallucinatory symptoms
  2. Mixed delirium–> variable course with alternating hyperactive and hypo active features…majority of patients fall into this category
  3. Hypo active delirium–> characterized by excessive drowsiness and decreased LOC, may mimic depression
193
Q

How does the onset differ between

  1. Delirum
  2. Dementia
A
  1. Abrupt

2. Insidious

194
Q

How does the course differ between

  1. Delirium
  2. Dementia
A
  1. Fluctuating, usually reversible

2. Slowly progressive and usually irreversible

195
Q

How does the duration differ between

  1. Delirium
  2. Dementia
A
  1. Days to weeks

2. Years

196
Q

How does the level of consciousness differ between

  1. Delirium
  2. Dementia
A
  1. Hyper or hypo active

2. Affected in late stages

197
Q

How does attention span differ between

  1. Delirium
  2. Dementia
A
  1. Often affected

2. Affected in late stages

198
Q

How does memory differ between

  1. Delirium
  2. Dementia
A
  1. May be affected

2. Usually affected

199
Q

What tool can be used to assess delirium?

A

The Confusion Assessment Method (CAM)

Positive test argues strongly for delirium (LR +10.3) and negative test argues against it

Positive test requires both major criteria 1 and 2 and either of the minor criteria 3 and 4

  1. Acute onset and fluctuating confusion–> abnormal behaviours come and go with variable severity
  2. Inattention–> difficulty focusing/difficulty following conversation
  3. Disorganized thinking–> rambling, irrelevant, illogical conversation
  4. Sensorium change (altered LOC)–> agitated, hyper alert, lethargic, stuporous, or comatose

Also should get a baseline MMSE to monitor

200
Q

What investigations should you get to work up delirium

A
  1. Labs–> CBCD, lytes, urea, Cr, glucose, calcium, UA
  2. Imaging–> CXR, CT head
  3. Micro–> urine C&S, blood C&S (if any fever)
  4. Metabolic workup
  5. Cardiac workup
  6. Seizures workup
  7. Drug OD workup
  8. Meningitis workup
201
Q

What is the metabolic workup for delirium

A

TSH if suspect hyper or hypothyroid

AST, ALT, ALP, bili, INR, PTT, ammonia if suspect liver disease

Magnesium

Phosphate

202
Q

What is the cardiac workup for delirium

A

ECG

CK

Troponin if suspect ACS

203
Q

What is the seizure workup for delirium

A

EEG

204
Q

What is the drug OD workup for delirium

A

Med serum levels

Alcohol levels

Serum osmolality

205
Q

What is the meningitis workup for delirium

A

LP

206
Q

What should you do if delirium persists and no cause found on workup

A

Think through diagnosis again
Ask caregivers about prior baseline–> pre existing sun downing?
Consider dehydration, depression, urinary/fecal retention, alcohol or benzo withdrawal, abscess, sleep deprivation, environmental factors

Inadequate pain control has also been suggests as a precipitant of delirium

207
Q

How can you prevent delirium

A 
Ensure adequate oxygen, fluid and electrolyte balance 
Pain management
Reduction in use of antipsychotics 
Bowel and bladder function
Nutrition
Early mobilization 
Prevention of post op complications 
Appropriate environmental stimuli 
Treatment of symptoms of delirium
208
Q

How would you manage delirium overall (principles of treatment)

A
  1. Prevention
  2. Treat underlying cause
  3. Non pharmacological measures
  4. Pharmacological measures
209
Q

How long does delirium take to resolve

A

Can take days/weeks to resolve been after the precipitating cause is removed and treated

210
Q

What are some non pharmacological measures that can be used to treat delirium

A 
Reduce noise
Orient patient frequently 
Early mobilization 
Provide proper hearing and visual aids
Provide clock/calendar and familiar objects and people 
Supervision for meals
Restoration of day-night cycle (optimal light during day, dark at night)
Avoidance of unnecessary interventions
211
Q

What are some pharmacological treatments for delirium

A
  1. Neuroleptics–> for agitated patient–> haloperidol, loxapine, quetiapine etc
  2. Benzodiazepines–> may precipitate or worsen delirium and should generally be avoided except in patients with alcohol or benzo withdrawal or those with severe agitate delirium despite high doses of neuroleptics–> lorazepam
212
Q

What causes T1DM

A

Autoimmune destruction of beta cells–> insulin deficiency

Affects 0.5% of world population

213
Q

What causes T2DM

A

Peripheral insulin resistance, impaired regulation of hepatic gluconeogenesis, impairment of beta cell function (beta cell exhaustion and from glucose toxicity)
Affects 8% of US population but increasing in the young –> 35% lifetime risk for those born in year 2000

214
Q

What are the risk factors for T2DM

A

Family history
Older age
Obesity

215
Q

How does the first onset of T1DM usually present

A

Often presents with diabetic ketoacidosis–> N/V, polyuria, anion gap metabolic acidosis, ketones in blood and urine

216
Q

How does T2DM usually present?

What end organ damage do we worry about?

A

Usually asymptomatic, discovered on routine testing

If symptomatic–> polyuria, polydipsia, polyphagia, fatigue, blurred vision, poor wound healing, recurrent candidiasis

Peripheral numbness–> neuropathy
Loss of vision–> retinopathy
Microalbuminuria, proteinuria–> nephropathy
Angina–> CAD
Claudication or impotence–> peripheral vascular disease

217
Q

What should you look for on physical exam in the diabetic patient

A
  1. Fundoscopy in office, annual dilated pupil exam with slit lamp
    - -> looking for non-proliferative retinopathy–> microaneurysms, hard exudates (vascular leakage), soft exudates (Ischemic injury), macular edema
    - -> looking for proliferative retinopathy–> neovascularization of the retina or optic disc
  2. Sensory–> vibration, light touch
    - -> always check feet
  3. Orthostatic vitals–> autonomic neuropathy
  4. Evidence of CAD–> increased JVP, S4, displaced PMI, peripheral vascular disease (decreased peripheral pulses, bruits)
218
Q

What is the Ddx for hyperglycaemia

A
  1. Diabetes
  2. Drugs (corticosteroids, thiazides diuretics, protease inhibitors)
  3. IV fluids (D5)
  4. Other endocrine–> acromegaly, cushings, pheochromocytoma
  5. Stress (via catecholamines release)
  6. Other–> hemochromatosis, pancreatic exocrine insufficiency (CF, acute or chronic pancreatitis)
219
Q

How do you diagnose diabetes?

A
  1. Fasting glucose higher than 7 mmol/L
  2. 2 hour OGTT higher than 11.1 mmol/L
  3. HbA1c higher than 6.5%
  4. Random glucose higher than 11/L WITH SYMPTOMS
220
Q

What is a normal fasting glucose

A

4-7 mmol/L

221
Q

What is “pre diabetes”

A

Fasting glucose 6.1-6.9, OGTT 7.8-11, HbA1c 6-6.4%

222
Q

What labs would you order in the diabetic patient

A

CBC
Iron studies (hemochromatosis)
Lipase (pancreatitis)
Urine micro albumin and creatinine annually

223
Q

How do you treat T2DM

A
  1. Biguanides (metformin)
  2. Sulfonylureas (glyburide, gliclazide)
  3. Meglitinides (repaglinide)
  4. Thiazolidinedions (pioglitazone)
  5. Alpha-glucosidase inhibitors (acarbose)
  6. DPP4 inhibitors (linagliptin-trajenta)
  7. SLGT2 inhibitors (saxenda, canafligozin)
  8. GLP-1 analogues (liraglutide)
224
Q

What do biguanides do? SEs?

A

Metformin

“Insulin sensitizing”

Inhibit hepatic gluconeogenesis and increase peripheral uptake of glucose

Very low incidence of lactic acidosis

SEs: GI (diarrhea). Avoid in patients with renal disease because is 100% really excreted and risk of lactic acidosis increases

225
Q

What do sulfonylureas do? SEs?

A

Glyburide, gliclazide

Increase amount of insulin produced by the pancreas.

SEs: weight gain, hypoglycemia

226
Q

What do meglitinides do?

A

Repaglinide

Increases insulin secretion

NOT really excreted so better for patients with renal disease

More expensive

227
Q

What do Thiazolidinedions do?

A

Pioglitazone

Increase insulin sensitivity in the liver and muscle

Slightly less potent

Usually used in combo with older agents

Most expensive

SEs–fluid retention

228
Q

What do alpha-gluconidase inhibitors do?

A

Acarbose

Inhibit absorption of carbs by preventing breakdown in small intestine

SEs: bloating, diarrhea, gas

Used in combination

229
Q

What do DPP4 inhibitors do?

A

Linagliptin, trajenta

Increases GLP-1 (incretins) by inhibiting DPP4

230
Q

How do you manage T1DM insulin therapy

A

Calculate 0.5 U/kg/day in T1–> T2 dose needs vary greatly

Short acting insulting–> regular and lispro–> used at times of meals

Intermediate insulin–> NPH and lente

Long acting insulin–> glargine–> basal insulin level throughout day especially at night (to suppress liver gluconeogenesis)

Can be given through numerous subQ injections or continuous infusion

231
Q

What are the neuroglycopenic symptoms of hypoglycemia? What are the adrenergic symptoms?

A
  1. Neuroglycopenic–> CNS dysfunction–> headache, blurred vision, confusion, seizure, loss of consciousness
  2. Adrenergic–> epi release–> tachy, tachypea, diaphoresis, tremulousness, palpitations, anxiety
232
Q

What is the difference between T1DM and T2DM

A

Basically, T1DM the problem is at the pancreas and in T2 it is as the tissue cells in the body

233
Q

Why do you develop hyperglycemia in DKA/HHS

A

Insulin resistance (relative or absolute)
Increased glucagon
Increased catecholamines, cortisol, growth hormone

234
Q

What is the major issue in DKA?

A

Ketoacidosis

Absolute insulin deficiency–> switch to using fats for fuel–> ketogenesis–> ketoacidosis

235
Q

What is the major issue in HHS?

A

Osmotic diuresis

Relative insulin deficiency and increased in counter-regulatory hormones–> increased proteolysis, increased gluconeogenesis
Severe hyperglycemia
Glucose is an active osmole causing osmotic diuresis

236
Q

How do the following differ in DKA vs. HHS

  1. Glucose
  2. PH
  3. HCO3
A
  1. Glucose–> DKA higher than 14//HHS higher than 33
  2. pH–> DKA less than 7.3 (acidosis)//HHS higher than 7.3 (non acidodic)
  3. HCO3–> DKA less than 15 (getting used up)//HHS higher than 18
237
Q

How do the following differ in DKA vs. HHS

  1. Urine ketones
  2. Serum ketones
  3. Serum osmolality
A
  1. Urine ketones–> present in DKA//small in HHS
  2. Serum ketones–> present in DKA//none or small in HHS
  3. Serum osmolality–> variable in DKA//higher than 320 in HHS
238
Q

How do the following differ in DKA vs. HHS

  1. Anion gap
  2. What symptoms are present?
A
  1. Anion gap–> higher than 12 in DKA//variable in HHS

2. DKA–> symptoms of ketoacidosis//HHS–> symptoms of osmotic diuresis

239
Q

Why do people get DKA/HHS?

A

Almost always there is PRECIPITANT –> something that triggers the hormonal abnormalities

I.e increased catecholamines, increased cortisol, less insulin

240
Q

What is the number one thing to do first when treating DKA?

A

GIVE FLUIDS

241
Q

What are the general principles of treatment of DKA?

A
  1. Fluid resuscitation
  2. Avoidance of hypokalemia
  3. Correct the acidosis–> aim to CLOSE THE ANION GAP
  4. Maintain high/normal-glycemia (don’t bring BG down too much)
  5. Search for a precipitating cause
  6. Transition to SC insulin
  7. In kids, avoid cerebral edema
242
Q

How do you manage fluid resuscitation in DKA/HHS?

A
  1. GIVE FLUIDS UP FRONT
    - -> pretty much everyone can take 2L IVF
  2. Then, run patients at 150-200cc/hr as most have significant fluid deficit
  3. Once euvolemia achieved, can switch to maintenance fluids
  4. NS usually used up from but not ideal–> worsens acidosis–> balanced salt solution preferable–> switch to hypotonic fluid if Na becomes elevated
243
Q

What is the overall K balance in DKA/HHS?

A

Depleted

Due to osmotic diuresis and K+/ketoacid salt excretion

DKA–> 2-5mmol/kg deficit
HHS–> 4-6mmol/kg deficit

K is often normal on tests because it shifts out of cells due to acidosis, insulin deficiency and hyperosmolality

244
Q

How do you manage K balance in DKA/HHS?

A

Monitor lytes q2-3h

  1. If initial K less than 3.3–> not NOT start insulin until K is corrected–> give 40mEq IV immediately
  2. If initial K 3.3-5, run IVF with K added (20-40 mEq in 1L)
  3. If initial K above 5, don’t need to add K to initial fluids–> know that it will likely drop precipitously once the acidosis is corrected
245
Q

Why do we give insulin in DKA/HHS?

A

To CLOSE THE ANION GAP (not to lower blood glucose)

246
Q

How much insulin do we give to treat DKA/HHS?

A

Insulin IV infusion at about 5-10u/hour (0.14u/kg/hr)

Monitor CBG q1h, lytes 2-3h

Goal is to close the anion gap

247
Q

How do we titrate the insulin infusion based on blood glucose monitoring in DKA/HHS?

A

If AG is unchanged–> increased infusion

If AG decreasing–> can titrate the infusion down

If AG is still open but BG less than 15, START D5W

248
Q

When do you start adding D5W to fluids in DKA/HHS?

A

If anion gap is still open but BG is less than 15, start D5W

249
Q

What are the precipitating causes of DKA/HHS? What’s the memory tool?

A

The 7 Is:

*Insulin deficiency (“idiocy”)
*Infection–pneumonia, UTI, gastro etc
Iatrogenic–glucocorticoids
Inflammation–cholescystitis, pancreatitis
Ischemia or infarction–myocardial, cerebral, mesenteric, pulmonary
Intoxication–alcohol, drugs
Impregnation

250
Q

What labs/investigations should everyone presenting with DKA get?

A 
Thorough Hx/px
Pan cultures
CXR
ECG
Tox screen 
Liver enzymes, lipase
Beta HCG (pregnancy)
251
Q

What are the criteria for transitioning to SC insulin when managing DKA/HHS?

A

ANION GAP IS CLOSED

PH above 7.3, HCO3 above 15
Patient is tolerating normal diet (watch them eat!)
Daytime hours–> do not switch overnight

Ensure at least two hour bridge with subcutaneous insulin

Must start LONG ACTING as well as rapid or will go back into DKA

252
Q

What is the recommended dosing for SC insulin after treating DKA/HHA?

A
  1. New DM1–> 0.5-0.8 units/kg/day
  2. Known DM1–> restart basal and prandial dose with or without sliding scale; start at lower dosing until you’re sure they’re eating well
  3. Known DM2–> estimate basal insulin at 0.3 u/kg/day and consider restart or oral agents
253
Q

What should you bear in mind with treatment that is unique to HHS (versus DKA)

A
  1. More volume deplete–> fluids usually key treatment, must watch electrolytes as are also more K deplete
  2. Less acidodic–> need less insulin to close the anion gap
  3. Target a higher BG before assign D5W as these people tend to be used to running a bit hyperglycemic and may not be able to immediately handle normoglycemia
  4. Correct precipitating cause
254
Q

What is a basic approach to an ABG interpretation?

A
  1. What is the “emia”–> acidemia versus alkalemia
  2. What is the “osis”–> respiratory versus metabolic
  3. Appropriate compensation?
  4. What is the anion gap?
  5. What is the delta delta?
255
Q

Define shock

A

Inadequate tissue perfusion potentially resulting in end organ injury

256
Q

List the types of shock

A

Hypovolemic
Cardiogenic
Obstructive
Distributive

257
Q

Examples of causes of hypovolemic shock

A 
Hemorrhage
Dehydration
Vomiting
Diarrhea 
Interstitial fluid redistribution
258
Q

Examples of causes of cardiogenic shock

A

Myopathic (ischemia, infarction)
Mechanical
Arrhythmic
Pharmacological

259
Q

Examples of causes of obstructive shock

A

Massive PE (saddle embolus)
Pericardial tamponade
Constrictive pericarditis
Increased intra thoracic pressure (tension pneumo)

260
Q

Examples of causes of distributive shock

A 
Sepsis
Anaphylaxis 
Neurogenic 
Endocrinologic
Toxic
261
Q

What should you ask on history in a patient with shock

A

Pay particular attention to the risk factors for sepsis (pna, UTI, recent chemo, SSTIs)
Blood loss
MI
PE (cancer, immobilization, calf pain, recent surgery)
General PMHx
Meds

262
Q

What should you look for on physical of a patient with low BP/shock

A 
Vital
Assess volume status 
Cardiac and resp function 
Extremities 
Look for evidence of end organ dysfunction or hypo perfusion
263
Q

What are you looking for on foot exam in a patient with shock? Why?

A

WARM feet–> vasodilation–> distributive shock–> give fluids and other vasopressors

COLD feet–> vasoconstriction–> cardiogenic vs. Hypovolemic vs. Obstructive vs. Late septic–> give fluids and consider inotropes especially if suspect cardiogenic
–also check troponin and consider echo

264
Q

Describe how HR, BP, JVP, extremities respond in hypovolemic shock

A

HR increased
BP decreased
JVP down
Extremities cold

*look for visible hemorrhage or signs of dehydration

265
Q

Describe how HR, BP, JVP, extremities respond in cardiogenic shock

A

HR low, normal or high
BP low
JVP high
Extremities cold

*bilateral crackles on chest exam

266
Q

Describe how HR, BP, JVP, extremities respond in obstructive shock

A

HR up
BP down
JVP up
Extremities normal or cold

*depending on the cause, may see pulsus paradoxus, Kussmaul’s breathing, tracheal deviation

267
Q

Describe how HR, BP, JVP, extremities respond in distributive shock

A

HR up or down
BP down
JVP down
Warm extremities

*look for obvious signs of infection or anaphylaxis

268
Q

What investigations would you do in a patient presenting with shock

A
  1. Labs–> CBCD, extended lytes, urea, Cr, INR, PTT, liver enzymes, TSH, D dimer, lactate, CK, troponin, UA, random cortisol
  2. Micro–> blood, sputum and urine C&S
  3. Imaging–> depends on suspected source… CXR, AXR, echo, CT (I.e if abdo source suspected)
  4. ECG
  5. ABG
269
Q

How do you manage shock acutely

A 
ABC
Oxygen 
oximetry monitoring 
IV fluid resuscitation
Inotropes (dobutimine, milrinone)
Pressors (norepi, phenylephrine)
 Re-vascularize or thrombolytics for Ischemic events
270
Q

Define primary HTN

A

High BP in which all secondary causes are not present

Accounts for 95% of all cases

Genetic factors are though to contribute

Increased sympathetic output, angiotensin II and mineralocorticoids, renal injury may play a role

271
Q

Define secondary HTN

A

Pathogenesis of increased BP is related to an identifiable underlying condition

272
Q

What are the risk factors for essential HTN

A

Obesity
African American race
High salt intake (in salt sensitive patients)
Insulin resistance
High alcohol intake above 2 drinks per day
Family history–risk doubles if one parent is hypertensive

273
Q

What is hypertension a risk factor for

A 
Cerebrovascular disease
CAD
CHF
Afib 
CKD
PVD
Dementia 
Erectile dysfunction
274
Q

How common is white coat HTN

A

About 10% of adult population

275
Q

How do you dx HTN

A
  1. Elevated BP at home, office or pharmacy
  2. Schedule a dedicated HTN visit… If above 180/110, has HTN
  3. If not…
    A. and the patient has diabetes and an Automated office BP (AOBP) of above 130/80, proceed with further out of office measurement with an ABPM (or home series)… If above 135/80 as a daytime mean or above 130/80 as a 24 hour mean, they have HTN. If not, have white coat HTN
    B. And the patient does not have diabetes, and has an AOBP of above 135/85 then proceed with out of office measurement with ABPM or home series. See above. If they meet the above criteria, they have HTN. If not, they have white coat HTN.
    C. If the diabetic or non diabetic patient does not meet the above 130/80 // 135/85 criteria in the office on the dedicated visit, then they do not have HTN.
276
Q

When should you order a 24 hour ABPM

A

All patients with a potential HTYN dx should be considered for ambulatory monitoring

Disadvantages are cost and lack of availability

277
Q

What types of end organ damage would you want to asses for in a patient with HTN

A
  1. Cerebrovascular disease–> TIA/CVA, dementia
  2. Retinopathy
  3. Cardiac–> CHF, CAD, LVH
  4. Nephropathy–> albuminuria, CKD
  5. PVD–> intermittent claudication, ABI of less than 0.9, present of bruits
278
Q

How can you elicit information about end organ damage in a patient w HTN on history

A
  1. Neuro–> transient monocular blindness (TIA), limb/facial weakness (CVA), severe headache (hemorrhage)
  2. Cardiac–> chest pain (CAD), Dyspnea, leg edema (CHF)
  3. Retinal–> vision loss
  4. PVD–> claudication, AAA
279
Q

What are the grades of hypertensive retinopathy

A

1–> decreased artery to vein ratio

2–> focal arteriolar spasm

3–> FLAME HEMORRHAGES, cotton wool spots (Ischemic nerve damage), yellow exudates (plasma leakage)

4–> PAPILLEDEMA

280
Q

What labs would you order to work up a hypertensive patient

A 
UA
Blood chemistry 
Fasting glucose and maybe HbA1c
Fasting lipids 
Standard 12 lead ECG
Urine ACR in patients with diabetes or CKD
281
Q

What components make up the Framingham risk score

A 
Age
LDL cholesterol 
HDL cholesterol 
BP
Diabetes
Smoker
282
Q

What do the different risk stratification levels in the Framingham score mean

A

Low risk–> less than 10% risk of non fatal MI or CHD death within next 10 years

Moderate risk–> 10-20% risk

High risk–> more than 20% risk

283
Q

What are the non modifiable CV risk factors

A

Age
Male sex
Family Hx (less than 55 y males, less than 65 y female)

284
Q

What are the modifiable CV risk factors

A 
Smoking
Dyslipidemia
Dysglycemia 
HTN
Abdominal obesity (>35 inches males, >40 inches females)
Sedentary lifestyle 
Poor dietary habit
285
Q

Why do we treat people younger than 60 with HTN

A

Reduces risk of stroke by 40%

Reduces risk of coronary event by 14%

286
Q

Why do we treat patients older than 60 with HTN

A

Reduces overall mortality by 15%
Reduces CV mortality by 36%
Reduces incidence of stroke by 35%
Reduces coronary artery disease by 18%

287
Q

What is the target BP in patients over 80

A

Less than 150 from the HYVET trial

288
Q

What lifestyle modifications can help manage HTN

A
  1. Less than 2 g sodium per day
  2. Healthy diet with fruits and veg, low fat dairy, whole grains
  3. Regular physical activity
  4. Less than 14 drinks per week for men and 9 for women
  5. Maintenance of ideal body weight of BMI 18.5-24.9
  6. Waist circumference less than 102 cm for men and 88 for women

**most effective are exercise and dietary patterns

289
Q

What are the indications for starting meds in a HTN patient

A
  • dBP above 100 or SBP above 160 without macro vascular damage
  • dBP above 90 in macro vascular damage or CV risk factors
  • SBP above 140 in macro vascular damage
  • SBP above 160 in seniors
290
Q

What are the drugs used to treat HTN

A 
Thiazides diuretics
ACEi
ARB
Long acting CCB
Beta blocker--not as first line in age 60 or older

Can use a combo of any two of these as first line therapy–often thiazide and ACEi
Make sure to check renal function with ACEi/ARB
CHEP says start initially with mono therapy

291
Q

In a patient with HTN and stable angina what do you use?

A

Beta blocker
Long acting CCB
ACEi

292
Q

In a patient with HTN and recent ACS what do you use?

A

Beta blockers

ACEi

293
Q

In a patient with HTN and decreased LVEF what do you use?

A

ACEi
Beta blockers
Nitro/hydralazine
Aldosterone antagonist

294
Q

In a patient with HTN and non diabetic CKD what do you use?

A

ACEi/ARB
Thiazide
Loop for volume control

295
Q

In a patient with HTN and diabetes without nephropathy what do you use?

A

ACEi/ARB -or-
Thiazide -or-
ND-CCB

296
Q

In a patient with HTN and diabetes with nephropathy what do you use?

A

ACEi/ARB then ND-CCB

297
Q

Adverse effects of thiazides

A

Hypokalemia
Hyponatremia
Worsening gout

298
Q

Adverse effects of non-DHP CCB

A

Bradycardia

Constipation

299
Q

Adverse effects of DHP-CCB

A

Peripheral edema

300
Q

Adverse effects of beta blocker

A

Fatigue, erectile dysfunction, bradycardia, depression

301
Q

Name a CCB

A

Amlodipine

302
Q

When do you start to consider secondary HTN may be a cause

A

Severe or resistant HTN (requiring more than 3 drugs to control)

HTN in the very old or the very young–> new onset HTN in the elderly or age less than 30 with no family history and no obesity

Sudden increase in BP when previously controlled

Flash pulmonary edema with elevated BP

303
Q

What are the classes of causes of secondary HTN

A

Endocrine
Renal
Drugs
Other

304
Q

Endocrine causes of secondary HTN

A

Primary aldosteronism

Cushing syndrome

Hyperthyroidism

Hypothyroidism

Pheochromocytoma

305
Q

Symptoms of primary aldosteronism

A

Persistent hyperkalemia

Metabolic alkalosis

306
Q

Symptoms of cushings

A

Cushingoid face

Easy bruising

Thinning skin

Centra obesity

Proximal muscle weakness

307
Q

Symptoms of hyperthyroidism

A

Palpitations

Vision changes

Diarrhea

Heat intolerance

308
Q

Symptoms of hypothyroidism

A

Weight gain

Cold intolerance

Constipation

309
Q

Symptoms of a pheochromocytoma

A

Spells of tachy

Sweating

Headache

Pallor

Panic attacks

310
Q

What are the renal causes of secondary HTN

A

Renal artery stenosis

Parenchymal–> CKD, polycistic kidneys

Glomerular–>GN

311
Q

In what patient might you suspect renal artery stenosis

A

Acute rise in creatinine after ACEi/ARB

Moderate to severe HTN in patient with diffuse atherosclerosis

Repeated flash pulm edema

312
Q

What are some drugs that can cause secondary HTN

A

NSAIDs–including “coxibs”

OCP

Sympathomimetics–> cocaine, oral decongestants

Steroid based–> prednisone, fludrocortisone, anabolic

Calcineurin inhibitors–> cyclosporine, tacrolimus

313
Q

What are some “other” causes of secondary HTN

A

OSA–> snoring, daytime somnolence, headache, non restorative sleep

Coarctation of the aorta

314
Q

How do you investigate for

  1. Pheochromocytoma
  2. Primary aldosteronism
  3. Cushings
  4. Hyper/hypothyroid
A
  1. 24 hour urine metanephrines
  2. Serum renin, aldosterone, hypokalemia
  3. 24 hour urine cortisol
  4. TSH
315
Q

How do you investigate for

  1. OSA
  2. Coarctation of the aorta
  3. Renal artery stenosis
  4. Polycystic kidneys
A
  1. Overnight oximetry
  2. CXR, echo
  3. MR or CT angiogram, Captopril renal scan if eGFR is above 60
  4. Renal U/S
316
Q

What is a hypertensive crisis

A

SBP above 200, dBP above 120

317
Q

What is a hypertensive urgency

A

A hypertensive crisis that gets lower in 24-48 hours with NO end organ involvement

318
Q

What is a hypertensive emergency

A

A hypertensive crisis with END ORGAN involvement

319
Q

What are some signs of end organ involvement indicating a hypertensive emergency

A 
Neuro--> encephalopathy, stroke
Retina--> retinopathy
Cardiopulm--> acute LV failure, pulm edema, aortic dissection, ACS
Renal--> acute GN
Other--> hemolysis
320
Q

How does HTN affect cerebral blood flow auto regulation

A

Shifts the curve to the right so the range at which the brain is able to auto regulate is higher… Don’t want them to get too hypotensive actually

321
Q

What oral agents can be used to manage a hypertensive emergency

A

Captopril–not with renal disease
Labetalol
Clonidine
Hydralazine

322
Q

What IV agents can be used to treat hypertensive emergency

A

Work within minutes

Nitroprusside
NTG
Labetolol

323
Q

Ddx of mono arthritis

A

ICU RN

Infectious
Crystal 
Unclassified 
Rheumatologist (early stage... Unusual presentation)
Neoplastic
324
Q

Infectious causes of mono arthritis

A

Bacterial–> gonococci, staph, strep, syphilis, TB

Viral–> HIV, HBV, parvovirus, rubella, mumps, enterovirus, adenovirus

Fungal–> cryptococcus

OM

325
Q

Crystal causes of mono arthritis

A

Gout

Pseudo gout

326
Q

Unclassified causes of mono arthritis

A

Trauma

OA

Hemarthrosis –> coagulopathy, thrombocytopenia, trauma

Non arthritis–> bone (OM, avascular necrosis, fracture), soft tissue (tendinitis, ligament tear, bursitis)

327
Q

Rheumatologist causes of mono arthritis

A
  1. Seropositive–> polymyositis, palindromic rheumatism, SLE, scleroderma, RA
  2. Seronegative–> psoriatic arthritis, enteric arthritis, ankylosing spondylitis, reactive arthritis
  3. Sarcoidosis, polymyalgia rheumatica
328
Q

Neoplastic causes of mono arthritis

A

Chondrosarcoma
Osteoid osteoma
Mets

329
Q

What is the most common cause of septic arthritis in sexually active adults without other risk factors (like immunosuppression)

A

50% is due to gonococcal infection

More common in women

Less destructive and better outcome than non gonococcal arthritis

330
Q

What is a finding often found in gout

A

Tophi

331
Q

How can you distinguish joint diseases from soft tissue injuries in your assessment of mono arthritis

A

Soft tissue–active ROM is affected while passive is not

Joint–both active and passive ROM is affected

332
Q

What should you do to test if someone has septic arthritis

A

Tap the joint

Check synovial WBC count and percentage of PMNs as these provide the best utility while waiting for gram stain and culture

patients with mono arthritis have septic arthritis until proven otherwise!!!!*

333
Q

What should you send arthrocentesis fluid for when assessing mono arthritis

A

3Cs

Cell count with diff
Culture and gram stain
Crystals

334
Q

Does the presence of crystals rule out sepsis?

A

No

335
Q

Empiric treatment for septic arthritis

  1. if not at risk for STD
  2. If at risk for STD
A
  1. Vancomycin IV plus ceftriaxone IV

2. Nafcillin or ceftriaxone

336
Q

Causes of gout

A

Decreased urate excretion (90% of cases)–> renal disease, drugs (cyclosporine, alcohol, nicotinic acid, thiazides etc)

Increased urate production (10%)–> metabolic syndrome (obesity, HTN), increased metabolism (alcohol, hemolytic anemia, psoriasis), neoplastic (MPD, chemo, lymphoproliferative disorder)

337
Q

Precipitants of gout

A 
Surgery
Dehydration
Fasting
Binge eating
Binge drinking
Exercise
Trauma
338
Q

What is a test to check for gout

A

Tap the joint

24 hour urine Uric acid collection

Tophi aspiration

339
Q

Management of gout

A

Acutely–> NSAIDs (I.e naproxen), systemic corticosteroids, intra articulate corticosteroids, colchicine during acute attack

Long term–> purine restricted diet (low red meat, low seafood, high low fat dairy products, high fruit and veg), allopurinol

340
Q

In what conditions would you see a polyarthritis with a temperature above 40

A

Stills
Bacterial arthritis
SLE

341
Q

In what conditions would you see a polyarthritis with fever preceding arthritis

A 
Viral arthritis 
Lyme 
Reactive arthritis 
Stills 
bacterial endocarditis
342
Q

In what conditions would you see a polyarthritis with migratory arthritis

A 
Rheumatica fever
Gonococcemia 
Meningococcemia 
SLE
Acute leukaemia 
Whipple's
343
Q

In what conditions would you see a polyarthritis with morning stiffness

A

RA
Polymyalgia rheumatica
Stills

344
Q

In what conditions would you see a polyarthritis with pain disproportionally greater than effusion

A

Rheumatic fever
Familial Mediterranean fever
Acute leukaemia
AIDS

345
Q

In what conditions would you see a polyarthritis with effusion disproportionately greater than pain

A

TB arthritis
Bacterial endocarditis
IBD
Lyme

346
Q

In what conditions would you see a polyarthritis with symmetrical small joint synovitis

A

RA
SLE
Viral

347
Q

In what conditions would you see a polyarthritis with leukopenia

A

SLE

Viral

348
Q

In what conditions would you see a polyarthritis with positive RF

A 
RA (sens and spec 70%)
Viral arthritis 
SLE
Sarcoidosis
Systemic vasculitis
349
Q

In what conditions would you see a polyarthritis with positive ACPA (anti cyclic cirtullinated peptide antibodies)

A

RA–not sensitive but highly specific

Internal Medicine General (4 decks)

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