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Clin Med II > ID Diagnosis > Flashcards

ID Diagnosis Flashcards

1
Q

What are the tests to diagnose HIV?

A

4th gen ELISA

confirm w/ western blot

PCR

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2
Q

What does HIV primary infection look like?

A

Fever, malaise, N/V/D, maculopapular rash, neuro sx

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3
Q

What labs do you want to monitor for HIV?

A

every 3-6 mo monitor:

CD4 cell count and HIV RNA

CBC

Chemistries

Liver, kidney, lipids, fasting glucose, HbA1c

Annual STIs, Hep B, C, HSV and cancer

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4
Q

Classic triad of RMSF

A

Classic triad: fever, headache & rash

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5
Q

Incubation of RMSF

A

2-14 d

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6
Q

Rash beings on ankles/wrists, palms/soles, spreads centrally, maculopapular, bit by tick

A

RMSF

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7
Q

What would labs for RMSF show?

A

eukopenia, thrombocytopenia

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8
Q

small painful ulcers on an erythematous base

A

HSV-1 & 2

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9
Q

large, shallow ulcers

A

CMV

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10
Q

ulcerations with exudate at

the base

A

Aphthous stomatitis

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11
Q

Kaposi’s sarcoma

A

associated w/ herpes virus

ca of enfothelium

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12
Q

Bacillary angiomatosis causative organism

A

Bartonella henselae

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13
Q

How is malaria transmitted?

A

Transmitted by female mosquito (Anopheles) → humans (intermediate host)

Can be transmitted via blood or to fetus but more rare

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14
Q

Epidemiology of malaria

A

MC Africa
South America

Malaria-endemic areas develop resistance to clinical dz slowly w/ age (quicker w/ higher intensity

*Resistance is to clinical manifestation NOT infection

Pregnant women more susceptible and lose resistance to infection

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15
Q

What to look for in labs if concerned about malaria

A

Anemia (Hgb <13)

Thrombocytomepia (<100K)

Leukopenia

↑ AST and ALT

↑ Creatinine

Microscopy- blood thin (species) & thick smears

Rapid Diagnostic Test

PCR

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16
Q

What type of malaria is the main cause of severe clinical malaria and death?

A

Plasmodium falciparum

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17
Q

How often is fever present for P vivax and P ovale?

A

every 2 days

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18
Q

How often is fever present for P malariae

A

every 3 days

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19
Q

What patient population is protected from P. vivax and why?

A

Duffy Ag absent in West African populations

Pts must have duffy antigen on their RBC in order for P. vivax to bind and invade

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20
Q

Where is Babesiosis MC seen?

A

New England, Wisconsin & Minnesota

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21
Q

What is the parasite that causes Babesiosis?

A

B. microti

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22
Q

How is Babesiosis transmitted?

A

Tick Ixodes scapularis (same as lyme)

*requires >24 hr of attachment

Can also be transmitted via blood transfusion

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23
Q

Microscopic exam of blood → “Maltese cross” pattern

Flu-like illness- fever, chills, fatigue, HA (lasting wks to mo)

A

Babesiosis

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24
Q

May be asymptomatic in children

Loose, foul-smelling stools

Steatorrhea (fat malabsorption)

Cramping, bloating, nausea

Anorexia, malaise, weight loss

No blood in stool

Chronic: steatorrhea, growth impairment

A

Giardia Intestinalis

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25
Q

How is Giardia Intestinalis transmitted?

A

drink contaminated fresh water (beaver fever)

1-4 wk incubation

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26
Q

Gradual onset

Liver abscess → sx >4 wk, fever, abd pain, hepatomegaly, jaundice, cough due to diaphragm irritation

Amebic dysentery and colitis - fever w/ bloody diarrhea, cramping, abd pain, weight loss

A

Amoebiasis

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27
Q

Amoebiasis etiology

A

Entamoeba histolytica

28
Q

Amoebiasis transmission

A

Fecal oral transmission

Invades mucosa of large intestine and thickness of intestinal wall → perforation or peritonitis and can get into blood stream→
If gets into portal circulation goes to liver

29
Q

Watery diarrhea

Dehydration, weight loss, abd pain, N/V

A

Cryptosporidiosis

30
Q

Cryptosporidiosis peak seasons

A

late summer and early fall

31
Q

Cryptosporidiosis transmission

A

Outbreaks in day care centers

Zoonotic transmission: farmers and animal handlers

Waterborne infection: swimming pools, public drinking water

32
Q

Winterbottom’s sign: posterior cervical adenopathy

Intermittent fever: due to antigenic variation

CNS involvement:
Diurnal somnolence, nocturnal insomnia, constant HA, behavior changes→ DEATH

Gambial HAT → mo to years

Rhodesian HAT→ wks to mo

A

Human African Trypanosomiasis (HAT)

“Sleeping Sickness”

33
Q

Human African Trypanosomiasis (HAT) epi and eti

A

sub-Saharan Africa
Trypanosoma brucei gambiense (West African)

Trypanosoma brucei rhodesiense (East African)

34
Q

How is Human African Trypanosomiasis (HAT) tranmitted?

A

Transmitted to human by Tsetse flies

35
Q

Chagoma: indurated lesion at site of parasite entry

Romaña’s sign when conjunctiva is port of entry

Fever, facial edema

Severe myocarditis w/ ECG changes

Chronic: dilated, megacolon, cardiomyopathy

A

Chagas Disease

36
Q

How is Leishmaniasis transmitted?

A

Sandfly Vector

37
Q

Fever, weight Loss

Hepatosplenomegaly

Pancytopenia
Hypergammaglobulinemia
Hyperpigmentation (“Black Fever”)

A

Kala-azar

Visceral Leishmaniasis (VL)

38
Q

Kala-azar

Visceral Leishmaniasis (VL) etiology

A

L. donovani (Asia-Africa

L. infantum (southern Europe)

L. chagasi (Brazil)

39
Q

Mucocutaneous Leishmaniasis (ML) etiology

A

L. braziliensis (Central/South America)

40
Q

What type of endocarditis is most likely to have peripheral manifestations?

A

Subacute Bacterial Endocarditis

41
Q

What are peripheral manifestations of infectious endocarditis?

A

conjunctival petecchiae

splinter hemorrhages

Osler’s nodes (pain, fingers and toes)

Janeway lesions (macules on palms and soles)

Roth’s spots (retinal hemorrhages)

42
Q

What pt pop is most likely to get SBE and what is the etiology of it?

A

Pts who recently had dental procedure or who have underlying valve abnormality

MC = Viridans Streptococci (part of oral flora)

43
Q

What pt pop is most likely to get ABE and what is the etiology?

A

MC w/ IVDU

S. aureus**

44
Q

What type of bacteria is most likely to be the cause of Cx neg endocarditis and why?

A

Coxiella burnetti or Chlamydia psittaci bc it doesnt grow well for cx

45
Q

What bacteria is most likely the cause of prosthetic valve endocarditis if presentation is <60 days from surg?

A

S. aureus or S. epidermidis

46
Q

What bacteria is most likely the cause of prosthetic valve endocarditis if presentation is >60 days from surg?

A

viridans streptococci

47
Q

What valves are MC involved in infective endocarditis?

A

Mitral MC then aortic

Tricuspid MC in IVDU

48
Q

What bacteria is associated w/ high morbidity w/ CHF and emboli?

A

Coag neg staph → S. lugdunensis

49
Q

Pathogenesis of NBTE

A

Endothelial cell damage, hypergoagulability (less common in US)

RF: valvular dz, malig, CT d/o, intracardiac catheter, prolonged febrile illness, persistent fetal circulation

50
Q

Pathogenesis of Transient bacteremia

A

MC in US Turbulent flow → high pressure flow, structural abnormality (regurg or narrow) and bacteremia (valvular adherence)

51
Q

What baseline labs should you get for pt presenting w/ fever and neutropenia?

A

CBC

Liver and renal function tests

Urinalysis, blood and urine culture

CXR

52
Q

What pt pop is at risk for Neutropenia and Defects in Phagocytic Defenses?

A

Post chemotherapy or other myelosuppressive therapy, bone marrow transplant recipients, acute leukemics

Risk of infection is significant at ANC <500

53
Q

What pt pop is at risk for infections due to defects in Cellular Immunity?

A

Pts w/ AIDs, Hodgkin’s lymphoma, monoclonal Ab therapy and LT corticosteroid use

Infection due to opportunistic pathogens

54
Q

What pt pop is at risk for infections due to Defects in Humoral Immunity?

A

Pts w/ gammaglobulinemia, Multiple Myeloma, CLL with hypogammaglobulinemia, splenectomized patients, sickle cell disease

55
Q

what organisms are pts w/ Pts w/ gammaglobulinemia, Multiple Myeloma, CLL with hypogammaglobulinemia, splenectomized patients, sickle cell disease at risk for?

A

Offending organisms are encapsulated, pyogenic bacteria: S. pneumoniae, H. influenzae

56
Q

What infections is HIV pt w/ CD4 <100 at risk for?

A 
Cryptococcal Infections
MAI
CMV
Toxoplasma
Cryptosporidium
57
Q

What infections is HIV pt w/ CD4 <200 at risk for?

A

PJP

58
Q

What is qSOFA criteria?

A

RR>22, AMS, SBP <100 mmHg

qSOFA ≥ 2 IDs pts w/ suspected infection who are likely to have a prolonged ICU stay or to die in the hospital

59
Q

What type of bacteria is most likely to cause sepsis and why?

A

Endotoxin bacteria more likely to cause sepsis (due to cell wall component on gram negs)

60
Q

Pathophys of sepsis

A

Life-threatening organ dysfn caused by a dysreg host response to infection

Bacteria invade tissue → macrophages are triggered and released causing pro and antiinflam mediators to respond

Sepsis occurs when proinflam mediators > anti and they exceed the boundaries of the local enviro

61
Q

MC cause of septic shock

A

“Any source of infection→ MC is pneumo, intra-abd infection, UTI bacteremia

MC G neg: E.Coli, Klebsiella, pseudomonas, enterobacter

MC G pos: Staph aureus, Strep pneumo

MC Fungi: candida”

62
Q

Define septic shock

A

Sepsis w/ circulatory and cellular/metabolic abnormalities profound enough to substantially ↑ mortality

(type of distributive shock bc of hypotension)

63
Q

Criteria for septic shock

A

At least 1 of the following:

Persistent hypotension after fluid resuscitation and requiring vasopressors to maintain MAP >65 mmHg

Serum lactate level >2 mmol/L

64
Q

W/u for septic shock

A

ID infection source: PE, blood cx, urine cx, resp cx, CXR, CT

CBC, CMP, LFT, coags, lactate, ABG

Assess preload (CVP, US)

65
Q

What do you expect to see on w/u for DIC?

A

PT/INR ↑ (extrinsic coagulation factors)

aPTT ↑ (intrinsic coagulation factors)

Fibrinogen ↓ (can be high during early sepsis)

D-Dimer ↑

Platelets ↓ (Thrombocytopenia)

Clin Med II (19 decks)

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