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USMLE Step 1 > Cardio, Respi, Renal Block > Flashcards

Cardio, Respi, Renal Block Flashcards

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USMLE® Step 1 flashcards
1
Q

What are the different kinds of RNA polymerases seen in eukaryotes and prokaryotes?

A

Eukaryotes:

RNA polymerase I
-function restricted to nucleolus
-synthesize template for rRNA
NB: nucleolus is primary site of ribosomal subunit maturity and assembly. In malignant cells, large nucleus composed of prominent basophilic nucleoli seen
RNA polymerase II
-most regulated of all RNA polymerases by transcription factors
-synthesizes mRNA, snRNA, miRNA
RNA polymerase III
-synthesizes small RNA e.g. tRNA, 5s rRNA

Prokaryotes:
JUST RNA polymerase (multisubunit complex)
-makes all 3 kinds of RNA

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2
Q

Which drugs influence RNA polymerase functions?

A

A-amanitin in death cap mushrooms

  • blocks RNA polymerase II
  • causes severe hepatotoxicity

Rifampicin
-blocks RNA polymerase (multisubunit complex) in prokaryotes

Actinomycin-D (antitumor and antibacterial)
-blocks RNA polymerases in both prokaryotes and eukaryotes

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3
Q

How does silicosis present?

A

Hx

  • occupational exposure e.g. miner, sandblaster
  • chronic cough, hemoptysis, dyspnea, chest pain
  • ***risk of TB and bronchogenic CA

PE

  • fine crepitations at ULs (asbestos from roof affects base, coal and silica from earth affect roof)
  • UL pulmonary nodules, hilar adenopathy with ‘eggshell’ calcifications

Ix
-histology: bifringent silica particles surrounded by fibrous tissue

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4
Q

What is the Pathophysiology of Silicosis?

A

Silica affects macrophage function (cell-mediated immunity)

  • causes macrophage release of fibrogenic factors
  • disrupts phagolysosomes, thereby releasing viable bacteria and lysosomal enzymes extracellularly
  • these cause interstitial fibrosis (ILD) and predisposition to mycobacteria infections
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5
Q

What are the features of a Histoplasmosis infection?

A

Non-immunocompromised: asymptomatic or self-limiting pulmonary disease

Immunocompromised:

  • systemic histoplasmosis (fever, weight loss, lymphadenopathy),
  • ulcerative tongue lesions, hepatosplenolegaly,
  • tuberculous features like pulmonary infiltrates, hilar adenopathy, cavitatory lesions in lung ULs if chronic, **macrophages filled with round yeasts on cytology (survives intracellularly)
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6
Q

Where is a thoracocentesis performed?

A
  • Insertion of needle just above superior margin of rib to avoid subcostal neurovascular bundle.
  • risk of injury to smaller collateral branches still persists
-Regions are between inferior margins of visceral and parietal pleura;
At the midclavicular line:
6th - 8th rib
At mid-axillary line:
8th - 10th rib
At paravertebral line:
10th - 12th rib
  • Needle inserted higher than landmarks –> penetrating lung injury.
  • Needle inserted lower–> penetrating liver trauma (R), splenic/bowel trauma (L)
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7
Q

What are the cell types seen in respiratory epithelium?

A

CONDUCTING ZONE

Tracheobronchial tree:
- pseudostratified ciliated columnar epithelium

Bronchi and large bronchioles:
-goblet cells –> mucin producing

Terminal bronchioles:
-Club cells –> secretory, and regenerative source of ciliated cells in bronchioles

RESPIRATORY ZONE

respiratory bronchioles:
-ciliated cuboidal epithelium (cilia terminate here)

alveolar ducts and alveoli:
-simple squamous epithelium
largely Type I Pneumocytes –> thin for gas exch.
some Type II Pneumocytes –> regenerate alveolar lining during lung damage, precursors for Type I cells, surfactant production.
some alveolar macrophages–> derived from fetal monocytes,clear inhaled debris.

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8
Q

What is the pathophysiology and presentation of Fabry disease(a type of lysosomal storage disorder)?

A

Pathophysiology:

  • X-linked recessive
  • alpha-galactosidase A deficiency
  • G3b accumulation in dorsal root, autonomic ganglia, cardiac myocytes, glomerular cells and vascular smooth muscles

In adolescence

  • neuropathic pain and hypohydrosis exacerbated by exercise, stress, fatigue.
  • Angiokeratomas and telangiectasias in clusters over groin, buttocks, umbilicus

In adulthood

  • TIA,stroke
  • cardiac disorders e.g. LVH
  • Glomerular diseases(proteinuria), renal failure
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9
Q

Hepatomegaly presents in which lysosomal storage diseases?

A

Present

  • Gaucher disease
  • Niemann-Pick disease
  • Hunter-Hurler syndrome

Absent

  • Fabry disease
  • Tay-sachs disease
  • Krabbe disease
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10
Q

What is the pathogenesis and presentation of Neurofibromatoses type 1 and 2?

A

NF1:

  • AD; mutations in NF1 gene on chr 17
  • Neurocutaneous disorder, unlike NF2
  • skin: cafe-au-lait spots, cutaneous neurofibromas, *neurofibrosarcoma (malignant nerve sheath tumor) can develop from neurofibromas
  • eyes: optic gliomas, Lisch nodules (iris hamartomas)
  • others: phaeochromocytoma

NF2:

  • AD; mutations in NF2 gene on chr 22
  • nil cutaneous features
  • bilateral acoustic schwannomas, juvenile cataracts, meningiomas, ependymomas
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11
Q

What are the 2 types of asthma?

A

Allergic (extrinsic)

  • suspect when non-allergic causes (see below) ruled out
  • triggered by allergens like food (esp in children) and aeroallergens e.g. seasonal pollen, mold spores, animal dander, dust mites.

Non-allergic (intrinsic)
-triggered by exercise and/or stress, aspirin use, pulm infection, viral URIs, inhalation of irritants e.g. cig smoke

Patients present with paroxysmal breathlessness and wheezing when young

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12
Q

What are the pathological findings in asthma?

A

Sputum sample:

  • eosinophils (granule containing cells)
  • charcot-leyden crystals (double pointed needle-like crystals from eosinophil breakdown)
  • curschmann spirals (shed epithelium forms whorled mucus plug)
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13
Q

What is the process of cardiac outflow tract formation?

A

-Truncus arteriosus rotates
-truncal and bulbar ridges appear and SPIRAL
-ridges fuse to form aorticopulmonary septum
This forms ascending aorta and pulmonary trunk

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14
Q

What is the pathogenesis and presentation of TGA?

A
  • Conotruncal deformity
  • Due to failure of aorticopulmonary septum to spiral (linear AP septum results)
  • aorta lies anterior and connects to RV; pulmonary trunk lies posterior and connects to LV
  • 2 parallel circulations
  • not compatible with life unless L->R shunt e.g. PFO, VSD, PDA exists

Presentation

  • normal infant at birth
  • at age 1-3days, onset of cyanosis, tachypnea, tachycardia due to PDA closure
  • machinery murmur +/- (PDA patency)
  • raised lactate
  • DEATH within first few months unless shunt created.
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15
Q

What is Persistent Truncus Arteriosus?

A
  • Failure of conotruncal septation
  • presentation: cyanosis and respiratory distress
  • ECHO: single arterial trunk, overriding large VSD
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16
Q

Explain the immunologic process to combat Mycobacterium Tuberculosis.

A
  • M.tuberculosis is an intracellular organism that survives in non-activated macrophages.
  • combated by cell-mediated immune process
  • CD4+ TH1 cells and macrophages play a key role
    • CD4+ T cells activated by APCs
    • resultant TH1 cells secrete IFN-gamma to activate macrophages
    • macrophages secrete TNF-a to form granulomas: walling off immune reaction consisting of Langhans multinucleated giant cells, epithelioid cells fibroblasts and collagen.
    • caseating granuloma allows macrophages in necrotic centre to kill off bacteria
17
Q

What investigation is necessary to prevent a serious side-effect of Anti-TNF-a drugs?

A

test for latent TB = PPD

  • TNF-a produced by macrophages maintains granulomas
  • Anti-TNF-a can cause granuloma breakdown and disseminated disease.
18
Q

How do kidneys form embryologically?

A
  • urogenital ridge forms in intermediate mesoderm
  • nephrogenic cord develops from UG ridge
  • from nephrogenic cord, 3 sets of sequential nephric systems form:
    1) pronephros- from cephalic nephrogenic cord, later regresses
    2) mesonephros - from midportion of nephrogenic cord, interim kidney, permanent for males as wolffian duct (later ductus deferens and epididymis), regresses in females forming vestigial Gartner’s ducts
    3) metanephros
  • true kidney, permanent.
  • develops from ureteric bud
  • ureteric bud sprouts from caudal portion of mesonephric duct
  • ureteric bud penetrates sacral mesoderm, inducing formation of metanephric blastema (metanephric mesoderm)
  • signals exchanged between bud and blastema help differentiate structures
  • **Aberrant interaction between them produces congenital renal malformations
19
Q

Which structures in adult kidneys develop from ureteric bud and metanephric blastema?

A

metanephric blastema:

  • glomeruli
  • Bowman’s space to DCT

Ureteric bud:

  • Entire collecting system
    • collecting tubules and ducts
    • renal calyces
    • renal pelvis
    • ureters
20
Q

What are the different categories of grafts ?

A

Autograft - from self e.g. Ross procedure
Isograft - from twin or clone e.g. Bone marrow, Kidney transplants
Allograft - from nonidentical individual of same species e.g. heart, liver, kidney
Xenograft - from different species e.g. bovine/porcine heart valve replacements

21
Q

What are the different types of transplant rejection?

A

Categorized by acquity:

1) Hyperacute
- within mins to hours,
- preformed antibodies in recipient against donor antigens,
- widespread thrombosis of graft vessels seen with ischemia and fibrinoid necrosis
- Graft MUST be removed

2) Acute
- weeks to months
- exposure to donor antigens causes activation of humoral and cellular immunity
- vasculitis of graft vessels with dense lymphocytic infiltrate
- reversed/prevented with immunosuppresion

3) Chronic
- months to years
- refractory to immunosuppression and w/o precipitating factors e.g. active acute rejection, drug toxicity
- chronic low-grade cellular and humoral immune response to foreign antigens
- parenchymal fibrosis and later graft atrophy, arteriolosclerosis

22
Q

What are the key findings in chronic renal allograft rejection?

A
  • worsening HTN
  • rising Cr
  • proteinuria
  • graft atrophy
23
Q

How do the differing anatomies of L and R renal veins pose a problem?

A

R renal vein

  • short course
  • runs anterior to renal art. before draining into IVC
  • R gonadal vein drains directly into IVC

L renal vein

  • long course
  • runs anterior to renal art., crosses aorta under SMA, then drains into IVC
  • L gonadal vein drains into L renal vein, NOT IVC directly
  • **Pressure in L renal vein generally higher due to compression between aorta and SMA (“nutcracker effect”) or L sided retroperitoneal/abdominal mass
  • flank pain
  • hematuria
  • varicoceles: of pampiniform plexus of L testis (L gonadal vein insufficiency)
24
Q

What is the management of a GBS +ve mother?

A
  • prenatal screening at 35-37wks gestation for vaginal / rectal GBS colonization
  • if +ve, intrapartum abx prophylaxis to prevent neonatal GBS sepsis, meningitis and pneumonia
  • first line: penicillin
    second line: ampicillin
  • abx given much earlier e.g. 30weeks serve to eliminate GBS temporarily
  • postnatal Igs to affected infants has no true efficacy
  • breastfeeding to continue as per normal;
    benefits: mucosal immune protection by IgA, superior nutritional content, promote proper GI development
25
Q

Describe a normal JVP trace and changes with certain pathologies.

A

3 positive waves (a,c,v) and 2 negative waves (x and y descents)
a wave - R atrial contraction ** absent in AF
c wave - R ventricular contraction causing TV to bulge
X descent - R atrial relaxation and downward displacement of TV **absent in TR
v wave - inflow of venous blood into RA against closed TV
Y descent - R atrium emptying into R ventricle

26
Q

What are the findings in a constrictive pericarditis patient?

A

H & P:

  • Radiation therapy to chest, TB (esp immigrants from endemic regions) or cardiac surgery
  • progressive dyspnea, orthopnea, PND
  • peripheral edema
  • ascites

Ix:
CVP - rapid and deep y descent, dip and plateau sign
CT - thickened and calcified pericardium

27
Q

What are the findings in HCM?

A

H & P:

  • FHx (including sudden death)
  • syncope on exertion
  • sudden death
  • S4
  • if HOCM: systolic murmur and MR (systolic anterior motion of leaflet

Ix:
CVP - prominent a wave
CT - thickening of interventricular septum *ventricular hypertrophy has septal predominance

28
Q

What is a common bias associated with new methods of early detection for diseases with poor prognoses?

A

Lead-time bias

-artificial increase in survival time due to early detection;
patients screened with more sensitive tests appear to live longer ONLY because disease detected earlier
-prognosis (period from disease onset to death) is actually unchanged
-e.g. new screening methods for lung/pancreatic CA
-solution: adjust survival according to disease severity at time of diagnosis ( “back-end survival”)

29
Q

What is the significance of hyperhomocysteinemia?

A
  • raised plasma level of homocysteine is an independent risk factor for thrombotic events (MI, stroke, VTE) and atherosclerosis
  • due to genetic mutations for critical enzymes or B6, B9 (Folate) and B12 deficiency
30
Q

How do pathological findings in Chronic bronchitis and Asthma differ?

A

Chronic Bronchitis

  • thickened bronchial walls
    • hyperplasia of goblet cells (mucus gland enlargement; Reid index > 50%)
  • lymphocytic infiltrates
  • squamous metaplasia of bronchial mucosa

Asthma

  • thickened bronchial walls
    • submucous gland enlargement
    • SM hypertrophy
  • eosinophilic and mast cell infiltrates
31
Q

How does a chronic bronchitis patient present?

A

H&P

  • Hx of chronic tobacco smoking, or exposure to pollutants, silica dusts and cotton
  • chronic productive cough of >3mo for >2years
  • late onset dyspnea
  • hypoxemia(shunting), hypercapnia (CO2 retention), wheezing, crackles

Ix

  • CBC: secondary polycythemia
  • CXR : Barrel chest (air trapping)
  • Spirometry: reduced FEV1/FVC

USMLE Step 1 (1 decks)

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