ID, HIV/MusSkel/ Renal Diseases Flashcards

1
Q

Sugical site infections are caused by which bacterias?

A
  1. MRSA - “superbug”
  2. Enterococci
  3. coliform
  4. clostridium perfringen
  5. P.aeruginosa
  6. candidia
  7. bacteroid fragilis
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2
Q

Which SSIs present as peritonitis or abscess after GI surgery

A
  1. P.aeruginosa
  2. candidia
  3. bacteroid fragilis
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3
Q

What are the Risk factors for SSIs

A
  1. Chronic illness
  2. Extremes of age
  3. Immunocompromise status
  4. DM
  5. Biofilm formation on prosthetics
  6. Virulent factors like capsule and enzymes produced by bugs
  7. Dirty surgical wounds with dead tissues
  8. Foreign objects
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4
Q

How are SSIs diagnosed?

A
  1. Elevated WBCs
  2. Poor blood sugar control
  3. Elevated inflammatory markers e.g. C-reactive proteins
  4. Positive bacterial culture
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5
Q

What is the gold standard for diagnosis of SSIs?

A

Positive bacterial culture

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6
Q

Bloodstream infections are caused by?

A
  1. CV line
  2. Catheter-associated
  3. Blood products
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7
Q

What are the s/s of bloodstream infectons?

A
  1. Nonspecific
  2. Fever, altered mental status
  3. Hemodynamic instability
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8
Q

Bloodstream infections are diagnosed by? whatis the treatment?

A

DX: positive blood cultures

TX: Abx and antifungal

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9
Q

Sepsis is?

A

Systemic inflammatory response- “cytokines storm”

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10
Q

Souces of sepis include?

A
  1. Abscess
  2. Infective endocarditis
  3. Bowel perforation
  4. UTI
  5. Prosthetics
  6. Endometritis
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11
Q

What are the signs and symptoms of sepsis?

A
  1. Fever, altered mental status,
  2. Septic shock
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12
Q

What is the diagnosis and treatment of sepsis?

A

DX: cultures

TX: Abx

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13
Q

This condition causes hyperactive muscle contractions

A

Tetanus

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14
Q

1.Tetanus is caused by?

A

Clostridium tetani- Gram+, spore forming anaerobic bacilli

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15
Q

Second most powerful toxin

A

Tetanospasmin

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16
Q

What is the MOA of Tetanospasmin?

A

blocks glycine [inhibitory NT] release from spinal cord. Glycine is needed to inhibit muscle contraction. This leads to continuous, uncontrolled muscle contraction.

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17
Q

Symptoms of tetanus include?

A
  1. Trismus (lockjaw) involves spasms of the jaw muscle and clenching of the teeth
  2. “Fixed smile” due to spasm of face muscles
  3. Opisthotonus involves muscle spasms that cause an arching of the back
  4. Spasmodic inhalation and seizures in the diaphragm and rib cage. This reduces ventilation leading to death
  5. Can be transmited by cutting umbilical cord with dirty instrument. Autoclave kills spores
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18
Q

Describe the treatment and prevention of tetanus

A
  1. Sedatives, muscle relaxants, and penicillin are used in treatment
  2. Tetanus toxoid is used in vaccination
  3. TDaP 2, 4, 6 , 18 months and 5 years of age
  4. Td vaccine “Booster shot” every 10 years
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19
Q

Early signs of tetanus are?

A

Spasm of jaw, facial and neck muscles (trismus/lockjaw, risus sardonicus)

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20
Q

In tetanus motor neurons of the spinal cord (anterior horn and brainstem become hyperactive because?

A

Toxin specifically attacks inhibitory (Renshaw) cells.

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21
Q

Typical pneumonia is caused by which bugs?

A
  1. Strep pneumoniae (adult)
  2. H. influenza
  3. S.aurus (hospitalized,)
  4. Klebsiella (alcoholic)
  5. PCP (HIV)
  6. Covid 19
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22
Q

patient with typical pna presents with?

A

Shaking chill, high grade fever, SOB, productive cough

Ventilator-associated

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23
Q

Atypical pna is caused by?

A

Mycoplasma pneumoniae “ wall-less”

“walking pnemonia”

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24
Q

Patient with atypical pneumonia presents with?

A

Mild symptoms like:

  1. sore throat
  2. non-productive cough
  3. headache
  4. X-ray shows diffuse infiltrates. C “X-ray looks worst than patient”. Often called walking pneumonia
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25
Q

M. pneumoniae are resistant to penicillin because?

A

it has no cell wall

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26
Q

Atypical pna is diagnosed by?

A

Elevated titer of cold agglutinin (IgM)

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27
Q

What is the drug of choice for atypical pna?

A

Erythromycin or tetracyclin

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28
Q

The condition in the cxr is most likely caused by?

A

Mycoplasma pneumonia

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29
Q

What is the diagnosis for patient with this

A

TB- Microscope slide shows AFB

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30
Q

TB forms cavitations at the apex of lung as opposed to the base because?

A

They are obligate aerobes

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31
Q

Latent TB

A

No symptoms, patient may never even know they are infected

About 90% of people who carry latent tuberculosis will never develop an active infection

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32
Q

Symptoms of clinical TB

A

Fever, night sweats, weight loss , hemoptysis

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33
Q

___________ is used in TB immunization

A

1Attentuated M. bovis

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34
Q

Miliary tuberculosis is?

A

The development of active tubercles throughout the body leading to Death

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35
Q

Positive Montoux test shows?

A

−Recent immunization

−Previous tuberculin test

−Past exposure to M. tuberculosis

−Need further tests (chest x-ray, sputum for AFB)

−Negative in AIDS

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36
Q

ABX affected by resistant TB

A

INH,pyrazinamide , rifampin

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37
Q

The mage shows a patient with?

A

TB

Apical lesions - trade mark of Tuberculosis

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38
Q

Graft from one person to another, may be related or unrelated, cadeveric or live

A

Allograft

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39
Q

Graft from animal to human. Most commonly heart valves- leftlet of mitral valve.

A

Xenograft

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40
Q

Graft from one identical twin to another

A

Isograft

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41
Q

Graft from one part to another part of same individual

A

Autograft

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42
Q

Antibody mediated (type II) rejection. Occurs within minutes after transplant

A

Hyperacute rejection

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43
Q

Cell mediated rejection due to cytotoxic T-cells reacting against foreign MHC. Occurs days after transplantation. Reversible with immunosuppressants e.g. cyclosporine

A

Acute rejection

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44
Q

Rejection that is T-cell and antibody mediated vascular damage. Occurs months or years after transplant

A

Chronic rejection

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45
Q

Graft-versus-host disease is?

A

Grafted immunocompetent T cells vs. irradiated immunocompromised host resulting in severe organ dysfunction.

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46
Q

Elevated number of circulating leukocytes in blood

A

Leukemias

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47
Q

Describe the pathophysiology of leukemia

A

Normal bone marrow elements are “pushed out” with leukemic cells leading to a decrease production of normal WBC, RBC and platelets

Anemia, petechiae, bruises, bone pain, infection, fever

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48
Q

What are the signs and symptoms of leukemias

A
  1. Anemia
  2. petechiae
  3. bruises
  4. bone pain
  5. infection
  6. fever
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49
Q

Acute leukemias

A
  1. Blasts predominate
  2. Children or elderly
  3. Excellent prognosis
  4. Short and drastic course
  5. ALL: Children; Most resp to chemo; Lympohoblasts (pre-B or pre-T)
  6. AML: Myeloblasts
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50
Q

Chronic Leukemia

A
  1. More mature cells
  2. Middle life range
  3. Longer, less devastating course
  4. CLL: Lymphocytes; lymphadenopathy
  5. CML: MC with Philadelphia chromosome; Myeloid stem cells “Blast crisis”
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51
Q

Rheumatoid Arthritis is?

A
  • Chronic, destructive ,systemic inflammatory arthritis
  • Characterized by symmetric involvement of both large and small joints.
  • RA causes synovial hypertrophy and pannus formation with resultant erosion of adjacent cartilage, bone and tendons.
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52
Q

Rheumatoid arthritis is most common in?

A

female 20-40 age

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53
Q

RA has high incidence with _______ serotype

A

HLA-DR4

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54
Q

Pannus is

A

abnormal growth of fibrous tissues

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55
Q

Patient with RA complain of?

A
  1. Insidious onset
  2. Morning stiffness improves with use
  3. Pain, warmth, swelling and decreased mobility
  4. Polyarthropathy
  5. Fatigue, anorexia, weight loss
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56
Q

Physical exam finding in RA

A
  1. Wrist, metacarpophalangeal and proximal interphalangeal (PIP) joints, ankle, knees, shoulder, hip, elbow and cervical spine (C1, C2)
  2. Distal interphlangeal joints (DIP) are spared in RA
  3. Ulnar deviation of the fingers, swan neck deformities of digits
  4. Extra-articular manifestations:
  • Vasculitis, Subcutaneous nodules
  • Pericarditis, pleuritis
  • Carpal tunnel syndrome
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57
Q

Evaluation of RA

A
  1. Rheumatoid factor (anti-Fc IgG antibody)
  2. Elevated ESR
  3. X-ray: narrowing of joint spaces and erosion, pannus formation
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58
Q

Treatment of RA

A
  1. NSAIDs
  2. Steroid
  3. methotrexate
  4. choroquine
  5. gold
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59
Q

Describe the pathophys of OA

A
  • Chronic, noninflammatory arthritis of movable joints
  • Degenerative joint disease- “wear and tear arthritis”
  • No systemic manifestation
  • Deterioration of articular cartilage
  • Osteophyte (bony spur) formation at joint surfaces.
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60
Q

Risk factors of OA

A
  1. Family history
  2. Obesity
  3. Previous joint trauma
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61
Q

Patieent with OA will complain of?

A
  1. Joint pain worsen by activity and weight bearing and relieved by rest
  2. Crepitus
  3. Decreased range of motion
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62
Q

Physical exam of a patient with OA will show?

A
  1. Involvement of weight bearing joints (hip, knee, lumbar)
  2. Also involve DIP, PIP and cervical
  3. Stiffness and marked crepitus of the affected joints
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63
Q

Evaluation of OA

A
  1. Normal ESR
  2. X-ray: ulcerated cartilage, narrowing of joints spaces, osteophytes , dense subchondral bone
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64
Q

Treatment of OA will include?

A
  1. Physical therapy
  2. Weight reduction
  3. NSAID
  4. Intra-articular steroids for temporary relief
  5. Replacement
65
Q

Metabolic condition causing recurrent attack of acute monoaticular arthritis. It results from intra-articular deposition of uric acid crystals and is more common in men.

A

Gout

66
Q

Hyperurecimia in gout is due to?

A

under excretion of uric acid

67
Q

Patient with gout will complain of?

A

Recurrent attack of acute monoaticular arthritis, awakening the patient at night with excruciating joint pain

68
Q

Physical exam of a patient with gout will show?

A
  1. Involves big toe- podagra
  2. Midfoot , knee, ankle, and wrist
  3. Spares hip and shoulder
  4. Red swollen and very tender affected joint
  5. Chronic => tophi (chunks of uric acid crystals that accumulate in and around joints)
69
Q

Evaluation of a patient with gout involves?

A

Joint fluid aspiration reveals needle shape crystals and elevated serum uric acid

70
Q

What is the treatment of gout?

A
  1. Uricosuric agent - probenecid
  2. Steroid
  3. Avoid thiazide/loop => hyperuricemia
  4. Allopurinol (xanthine oxidase inhibitor)- C/I in acute attack
  5. Colchicine
71
Q

Drug induced autoimune disorder commonly in women (90%)

A

SLE

72
Q

These 3 drugs can cause SLE

A
  1. INH
  2. procainamide
  3. hydralazine
73
Q

Patient with SLE will report what history

A
  1. Fever
  2. anorexia
  3. weight loss
  4. joint pain
  5. photosensitivity
  6. oral ulcer
74
Q

physical exam of a patient with SLE will reveal?

A
  1. Malar rash
  2. joint tenderness and inflammation
  3. pericarditis
  4. pleuritis
  5. neurological, renal and hematological abnormalities
75
Q

Evaluation of SLE involves

A
  1. Positive ANA (anti-nuclear antibody)
  2. Anti-DNA and anti-SM antibodies
76
Q

Treatement of SLE involves

A

NSAID

steroid

chloroquine

cyclophosphamide

77
Q

A poorly characterized disease with excessive bone turnover

A

Paget’s disease

78
Q

History and physical of paget’s disease

A
  1. Often asymptomatic
  2. Deep bone pain
  3. Tibial bowing, kyphosis and frequent fractures
  4. large cranial diameter “frontal bossing”
79
Q

X-ray in paget’s desease will show?

A
  1. Markedly expanded bony cortex
  2. Increase density, bowing
80
Q

This drug is the treatment for paget’s desease

A

Calcitonin

81
Q

Polymyalgia rheumatica is commonly seen in?

A

women

82
Q

Patient with Polymyalgia rheumatica will report a history of?

A
  1. Pain and stiffness of shoulder and pelvic girdle
  2. Fever, weight loss, joint swelling
  3. Great difficulty getting out of chair
83
Q

Physical exam in Polymyalgia rheumatica reveals?

A

No weakness

84
Q

Polymyalgia rheumatica Evaluation includes?

A
  1. Anemia
  2. Elevated ESR
85
Q

Treatment of Polymyalgia rheumatica

A

Low-dose prednisone

86
Q

Ankylosing Spondylitis is more common in?

A

Male

87
Q

Ankylosing Spondylitis is associated with HLA ______ subtype

A

HLA B27 ( human leukocyte antigen B27)

88
Q

Patient with ankylosing spondylitis presents with what history and physical findigs

A
  1. Symmetrical involvement of spine and sacroiliac joint
  2. Joint fusion (bamboo spine), uvetitis, aortic regurgitation
  3. Shortness of breath: restrictive lung disease
89
Q

Causes of Nephrolithiasis include?

A
  1. Positive family history
  2. Low fluid intake
  3. Gout
  4. RTA
  5. Hyperparathyroidism
90
Q

Types of stones in nephrolithiasis

A
  1. Calcium oxalalate
  2. Calcium phosphate
  3. Triple phosphate “staghorn stone”
  4. Uric acid
91
Q

Radiolucent kidney stone

A

Uric acid

92
Q

Kidney stone associated with UTI

A

Triple phosphate “staghorn stone”

93
Q

Kidney stone in patient with primary hyperparathyroidism

A

Calcium phosphate

94
Q

Radiopaque kidney stone formed in alkaline urine. It is idiopathic and the most common

A

Calcium oxalalate

95
Q

Evaluation of Nephrolithiasis

A
  1. Microscopic hematuria
  2. Altered urinary pH
  3. Plain X-ray
  4. Abdominal U/S
  5. IVP
  6. CT
96
Q

Treatment of Nephrolithiasis

A
  1. Hydration
  2. Analgesia
  3. Lithotripsy
  4. Neprolithotomoy
  5. Thiazide diuretics (Lower Ca++ conc in urine) for prevention
97
Q

What is the best test of renal function?

A

Creatinine clearance. It is approximately equals to GFR.

Creatinine clearance = ~GFR

98
Q

What test distinguishes prerenal from renal failure?

A

The fractional excretion of filtered sodium – FEFNa.

Decreased= prerenal,

Elevated =renal failure

99
Q

Glomerulonephritis

A
  1. Post beta-streptococcal infection- Cross reaction of antibodies
  2. Immune complex mediated
  3. Hematuria, proteinuria, HTN and edema
  4. Increase Cr
  5. Red cell cast
  6. Give steroid + immunosuppressive drugs
100
Q

Nephrotic sydndrome

A

A.Proteinuria > 3.5 g/day

B.Edema

C.Sodium retention

D.HTN

E.Hyperlipoproteinemia

F.Thromboembolic phenomenon and infections

101
Q

Nephrotic sydndrome is caused by?

A
  1. DM
  2. Neoplasia
  3. HIV
  4. Preeclampsia
102
Q

Goodpasture Syndrome

A

A.Hemoptysis and hematuria

B.Cross-reaction of antibodies

C.Progress to RF

103
Q

Interstitial nephritis

A

A.Allergic reaction to drugs

B.Autoimmune e.g. lupus

C.Infiltrative diseases

104
Q

Clinical presentation of Interstitial nephritis

A
  1. Proteinuria
  2. Decrease concentration ability
  3. HTN
  4. Reversible
105
Q

Hereditary nephritis (Alport’s syndrome)

A

A.Also have deafness and ocular problems

B.HTN

C.RF

106
Q

Treatment of Hereditary nephritis (Alport’s syndrome)

A

ACE inhibitor for some protection

107
Q

This renal condition is autosomal dominant and accompany Berry’s aneurysm that can cause SAH

A

Polycystic renal disease

108
Q

Fanconi syndrome is associated with defects in PCT functions leading to?

A
  1. Polyuria
  2. Metabolic acidosis due to loss of HCO3
  3. Skeletal muscle weakness due to loss of potassium
  4. Dwarfism and osteomlacia due to loss of phosphorous
  5. Vit-D resistant rickets
109
Q

This complication of fanconi syndrom is due to decreased Phosphate reabsorption

A

Rickets

110
Q

This complication of fanconi syndrom is due low HCO3- reabsorption

A

Metabolic acidosis (type-2 RTA)

111
Q

This complication of fanconi syndrom is due low Early Na+ reabsorption

A

High Distal Na+ reabsorption =>hypokalemia

112
Q

This renal disorder is immune complex mediated and is ascociated with a p ost beta-streptococcal infection and red cell cast

A

Glomerulonephritis

113
Q

This renal disorder is ascociated with Thromboembolic phenomenon and infections. It is caused by DM, neoplasm, HIV or preeclampsia.

A

Nephrotic sydndrome

114
Q

Patient with this renal disorder present with Hemoptysis and hematuria. Its is ascociated with Cross-reaction of antibodies Progressing to RF

A

Goodpasture Syndrome

115
Q

This renal disorder is ascociated with Allergic reaction to drugs, autoimune deseases such as lupus and infiltrative deseases. It is reversible

A

Interstitial nephritis

116
Q

This renal disorder is accompanied with deafness and occular problems

A

Hereditary nephritis (Alport’s syndrome)

117
Q

Pseudomembranous colitis

A
  1. By clostridium difficile
  2. Antibiotic-associated diarrhea
  3. Clindamycin, cephalosporins, quinolones and penicillin kill normal flora then opportunistic like C.diff invade
  4. 20% in hospitalized patient
  5. New multiple drug resistant strains have emerged
  6. F.C.diff produces two enterotoxins A and B
118
Q

signs and symptoms of Pseudomembranous colitis

A

Diarrhea and abdominal pain and distension

119
Q

Diagnosis of pseudomembranous coliis

A
  1. Toxins in stool
  2. Flexible sigmoidoscopy / colonoscopy
120
Q

Treatment of Pseudomembranous colitis

A
  1. D/C current antibiotic
  2. Fluid and electrolyte balance
  3. Oral vancomycin or metronidazole
121
Q

CD4 count for AIDS

A

≤200

122
Q

Normal CD4 count

A

500-1500

123
Q

HIV Laboratory diagnosis

A
  1. Look for antibodies against viral proteins
  2. Presumptive Dx made with ELISA “RULE OUT test”
  3. Positive results are then confirmed with Western blot assay “ RULE IN test”
  4. HIV PCR / viral load tests
  5. AIDS diagnosis £ 200 CD4 (N=500-1500)
124
Q

During latent phase, HIV virus replicates in?

A

lymph node

125
Q

Physical Examination in HIV

A
  1. Low grade fever, night sweat, weight loss
  2. Facial seborrhea
  3. Diffuse lymphadenopathy (like Mono)
  4. Splenomegaly
  5. Oral candidiasis “thrush”
  6. Herpes zoster infection
126
Q

Clinical features of HIV

A
  1. Asymptomatic
  2. Persistent fevers and chill
  3. Drenching night sweats
  4. Fatigue, arthralgias, myalgias
  5. Unintentional weight loss “HIV wasting syndrome”
  6. Depression, apathy, as early signs of HIV-related encephalopathy
127
Q

Bacterial Opportunistic infections in AIDS

A

−Tuberculosis, Mycobacterium avium-intracellulare

128
Q

Virus Opportunistic infections in AIDS

A

−Herpes simplex, varicella-zoster virus, cytomegalovirus

129
Q

Fungal Opportunistic infections in AIDS

A

−Thrush (candida) cryptococcosis , histoplasmosis, pneumocystis pneumonia

130
Q

Protozan Opportunistic infections in AIDS

A

−Toxoplasmosis, cryptosporidiosis

131
Q

Leading cause of death in HIV

A

Pneumocystis carinii

132
Q

Most common complain in HIV

A

Fever

133
Q

Most common finding with HIV patients presenting with headache, confusion and seizures

A

Toxoplasma -CT scan shows multiple ring-enhancing lesion

134
Q

This drug is treatment for HIV patient presenting with headach and seizures

A

Pyrimethamine and sulfadiazine- lifelong

135
Q

Diarhea in HIV patient caus be due to?

A
  1. Cryptosporidium , microsporidium , giardia, E.histolytica
  2. Colitis – CMV
  3. Proctitis “ gay bowel syndrome” with treponema, HSV and gonorrhea
136
Q

Fever in HIV patient

A
  1. Most common complain
  2. Blood culture should be drawn for bacteria, fungus, atypical mycobacterium (MAI) and CMV
  3. Assume Lymphoma when organomegaly and marked lymphadenopathy present
137
Q

Skin lesion in HIV patient

A
  1. Pruritus and folliculitis common
  2. Kaposi’s sarcoma–Nodular and dark purple lesions on head, neck, RT, GIT. Treat with interferon
138
Q

This drug is used to treat Kaposi sarcoma in HIV

A

interferon

139
Q

This drug is used to treat Candidal esophagitis “oral thrush” in HIV patients

A

fluconazole or ketokenazole

140
Q

This drug is used to treat esophageal herpetic ulcers in HIV pts

A

acyclovir

141
Q

This drug is used to treat Esophageal CMV ulcer ulcers in HIV pts

A

gancyclvir

142
Q

This drug is used to treat Idiopathic HIV ulcer in HIV pts

A

oral prednisone

143
Q

Dyspnea with progressive non-productive cough and diffuse interstitial infiltrates in a patient with HIV indicates?

A

a.Pneumocystis carinii pneumonia is leading cause of death

144
Q

Causes of pulmonary distress in HIV

A
  1. Pneumocystis carinii pneumonia is leading cause of death
  2. Tuberculosis ( -ve tuberculin test)
  3. Atypical mycobacteria – Mycobacterium Avium-Intracellulare (MAI)
  4. Disseminated fungal disease (cryptococcus, histoplasma , coccidiodes)
145
Q

CNS lesions in HIV

A
  1. Toxoplasma
  2. CNS lymphoma
  3. HS encephalitis
  4. CMV encephalitis
  5. Mycobacterial or fungal brain abscesses
  6. Cryptococcal meningitis
146
Q

Headache and meningeal signs indicates

A

Cryptococcal meningitis

147
Q

Dementia in HIV patient

A
  1. Early HIV encephalopathy with depression and apathy
  2. Paraparesis , incontinence and global dementia
148
Q

This drug is used to treat blindness due to CMV retinitis in HIV patients

A

Gancyclovir

149
Q

Hematological abnormalities in HIV

A
  1. ITP like thrombocytopenia
  2. Anemia of chronic disease
  3. Lymphocytopenia
150
Q

Reverse transcriptase inhibitor given for CD4<500

A

Azidotheymidine (AZT)

151
Q

HIV therapy

A
  1. Azidotheymidine (AZT) with CD4 < 500- Reverse transcriptase inhibitor
  2. With CD4 < 200 add pneumocystis prophylaxis- Trimethoprim-sulphamethoxazole
  3. Vaccination for pneumococci, influenza and hepatitis
  4. No live vaccine (polio, rubella) should be administered.
  5. High risk of TB
152
Q

Four Stages of Infection HIV:

A
  1. Flu-like (acute)
  2. Feeling Fine (Latent)
  3. Falling Count
  4. Final Crisis
153
Q

Trismus

A

(lockjaw) involves spasms of the jaw muscle and clenching of the teeth

“Fixed smile” due to spasm of face muscles

154
Q

Opisthotonus

A

involves muscle spasms that cause an arching of the back

155
Q

how do we kill spores in hospital?

A

autoclave

heats 120-160 degrees celsius x 1 hour

156
Q

diagnostic for c.diff?

A

Enterotoxins: Toxin A and Toxin B

157
Q

treatment for pseudomembranous colitis / c.diff?

A

Oral Vanc or metronidazolej/flagyl

-dc current abx; fluid and electrolytes

158
Q
A