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Boards Final Review > Respiratory + Musculoskeletal > Flashcards

Respiratory + Musculoskeletal Flashcards

1
Q

Child with nasal polyps?

A

Think cystic fibrosis!!

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2
Q

Adult with nasal polyps?

A

think TRIAD

  • asthma
  • nasal polyps
  • Aspirin induce bronchospasm
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3
Q

What is the histological appearance of nasopharyngeal carcinoma? Which population do you see nasopharyngeal carcinoma?

A

Pleomorphic keratin-positive epithelial cells (poorly differentiated squamous cell carcinoma) in a background of lymphocytes

**think EBV in african children or CHINESE ADULTS

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4
Q

What are the two main mediators of pain in the lungs?

A

bradykinin and prostaglandin E2

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5
Q

What are the 4 phases of lobar pneumonia?

A
  1. Congestion - dilate blood vessels increasing blood flow causing congestion and edema
  2. Red hepatization - exudate, neutrophils, hemorrhage filling alveolar air space [solid consistency – liver like change]
  3. Grey hepatization - degradation of RBCs within the exudate
  4. Resolution - lung heals by regeneration of lining that was damaged (regeneration by type II pneumocytes)
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6
Q

What is the most common cause of mortality in a patient with influenza virus?

A

Influenza virus weakens the immunologic defenses increasing the risk for a superimposed S. aureus and H. flu bacterial pneumonia, which is the major cause of death.

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7
Q

What are the most common causes of aspiration pneumonia and where in the lung does it commonly affect?

A

Anaerobic bacteria in the oropharynx

  • Bacteroides
  • Fusobacterium
  • Peptococcus

**most common causes RIGHT LOWER lobe abscesses

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8
Q

How does TB affect the brain?

A

Causes meningitis in the meninges at the BASE OF THE BRAIN - so you will see caseating granulomas at the base of the brain.

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9
Q

What cells in the alveoli release protease?

A

Neutrophils and macrophages in response to a small amount of inflammation that is always present – A1AT neutralizes the proteases preventing alveolar damage

[in smokers there is a ton of protease activity]

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10
Q

In patients with a-1-antitrypsin deficiency, where does A1AT accumulate?

A

Mutation causes a misfolding of the a1AT protein LEADING to accumulation in the ENDOPLASMIC RETICULUM of hepatocytes resulting in liver damage/cirrhosis.

[a1At stains pink with PAS POSITIVE]

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11
Q

How does histamine affect blood vessels?

A

Histamine induced vasodilation (at arterioles) and increased vascular permeability (at post-capillary venules)

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12
Q

What is the cause of late-phase reaction in asthma?

A

-cell damage, inflammation and present of major basic protein perpetuating bronchoconstriction

[early phase is due to histamines, leukotrienes, etc leaidng to bronchoconstriction]

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13
Q

Which patient population is usually seen with allergic bronchopulmonary aspergillosis?

A

Asthmatics and Cystic Fibrosis patients

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14
Q

What are the two important mediators for healing response of the body/lungs?

A

TGF-B and IL-10

[TGF-B from pneumocytes induces fibrosis]

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15
Q

What is Caplan syndrome?

A

Coal Workers’ Pneumoconiosis + rheumatoid arthritis

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16
Q

What is the result of macrophage uptake of silica in the lung?

A

Silica enters macrophage and then IMPAIRS FORMATION OF PHAGOLYSOSOME – It increases the risk of TB, seen in the upper lobes of the lung

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17
Q

What is hypersensitivity pneumonitis?

A

Granulomatous reaction WITH EOSINOPHILS in the lung due to inhaled organic antigens (ex. pigeon breeder’s lung) – generally resolves with removal of exposure, but chronic exposure can lead to interstitial fibrosis

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18
Q

What pressure in the pulmonary circuit defines pulmonary HTN?

A

MAP over 25mmHg

19
Q

What are the different features of pulmonary HTN?

A
  1. Atherosclerosis of pulmonary trunk (due to high pressure)
  2. Smooth muscle hypertrophy of pulmonary arteries
  3. Intimal fibrosis
  4. PLEXIFORM LESIONS – group of capillaries placed together – seen in severe, long standing disease
20
Q

Inactivation of which gene is associated with high risk of primary pulmonary HTN?

A

BMPR2 – inactivating mutations lead to increased vascular smooth muscle proliferation and plexiform lesions

21
Q

Regardless of etiology, what is the general underlying theme of acute respiratory distress syndrome?

A

Activation of neutrophils induces protease and free-radical mediated damage of type I and II pneumocytes

22
Q

What is the major component of surfactant?

A

Phosphatidylcholine (Lecithin)

23
Q

What are adverse effects of supplemental oxygen with neonatal ARDS?

A

increased risk of free radical injury…

  1. retinal injury – leading to blindness
  2. lung damage – leading to bronchopulmonary dysplasia
24
Q

What cell does bronchioloalveolar carcinoma arise from?

A

Clara cells [tall columnar cells replace the type I and II pneumocytes]

25
Q

Where does the trachea deviate in spontaneous vs tension pneumothorax?

A

Spontaneous pneumothorax - towards collapse

Tension pneumothorax - away from collapse

26
Q

What is the reason for blue sclera in osteogenesis imperfecta?

A

Exposure of the choroidal veins due to thinning of scleral collagen

27
Q

What are the 3 main features of osteogenesis imperfecta?

A
  1. multiple fractures of bone - resembling child abuse
  2. blue sclera
  3. hearing loss - due to fracturing of the small bones of the ear
28
Q

What is the relationship of osteopetrosis with carbonic anhydrase II mutation?

A

This is one of the most common genetic variants leading to osteopetrosis.

Acidic environment is necessary to remove calcium from bone during bone resorption. Carbonic anhydrase can produce H+ and bicarb where the H+ contributes to the acidic environment altering the environment by preventing osteoclast activity.

29
Q

What are the clinical features and treatment of osteopetrosis?

A
  1. bone fractures – thick, but weak due to imbalance of osteoblasts and clasts
  2. anemia, thrombocytopenia, leukopenia with extramedullary hematopoesis
  3. vision and hearing impairment due to impingement on cranial nerves
  4. hydrocephalus - due to narrowing of the foramen magnum
  5. Renal tubular acidosis - seen with the carbonic anhydrase II mutation b/c without the correct enzyme there is a lack of H+ secreted into the lumen to be excreted therefore it is retained in the blood

Treatment – bone marrow transplant b/c the osteoclasts are the problem and they are derived from monocytes, so if you replace the monocytes you should be able to reabsorb bone correctly

30
Q

What is the effect of rickets and osteomalacia on bone?

A

defective mineralization of osteoid from osteoblasts – lots of osteoid deposition but no mineralization with calcium due to vit D deficiency

31
Q

What is the histology of bone in Paget disease of bone?

A

Mosaic pattern of lamellar bone – fragile bone due to lack of sealing of bone together (erratic deposition)

32
Q

What are the complications associate with Paget’s disease of the bone?

A
  1. high output cardiac failure - due to production of AV shunts
  2. osteosarcoma – osteoblasts are producing a ton of bone at the end of the disease and if there is a mutation it can make them go crazy causing cancer
33
Q

Which part of bone is most commonly affected in children v adults with osteomyelitis?

A

Children – metaphysis

Adult - Epiphysis

34
Q

What type of necrosis is seen with osteomyelitis?

A

Liquefactive necrosis - lytic focus (abscess) aka sequestrum surrounded by sclerosis of bone (aka involucrum)

35
Q

What is the general cause of avascular (aseptic) necrosis? What are complications of avascular necrosis?

A

Ischemic necrosis of bone and bone marrow - seen in trauma/fracture, steroids, sickle cel disease, and caisson disease (nitrogen gas emboli)

Complication - osteoarthritis and fracture

36
Q

Where do osteochondromas form on bone?

A

Lateral projection of the growth plate (metaphysis) – bone is continuous with the bone marrow and b/c the lateral projection is from the growth plate where cartilage is located, there is a cartilage cap over the bone – which may rarely transform in to chondrosarcoma

37
Q

What is the ONLY tumor that arises from the epiphysis?

A

Giant cell tumor

38
Q

What cells does Ewing Sarcoma arise from?

A

Poorly differentiated cells derived from the NEUROECTODERM (which look similar to lymphocytes)

39
Q

What type of lesion does metastatic prostatic carcinoma create in bone?

A

osteoBLASTIC

40
Q

What is the hallmark of rheumatoid arthritis?

A

synovitis with the formation of a panus

Inflammation of synovium producing thick layer of granulation tissue (contains BV, fibroblasts and myofibroblasts) the myofibroblasts cause contraction leading to fusion of the joint (ankylosis) and deviations of movement

41
Q

What are the 3 skin associations of dermatomyositis?

A
  1. helioptrope rash - on upper eyelids
  2. malar rash - similar to SLE (watch out b/t this disorder also has positive ANA similar to SLE once again)
  3. Gottron papules - red papules on elbows, knuckles and knees
42
Q

What is the major difference b/c T cell involvement with dermatomyositis and polymyositis?

A

Dermatomyositis - CD4+ T cell infiltration (perimysial inflammation with perifascicular atrophy)

Polymyositis - CD8+ T cell (endomysial inflammation with necrotic muscle fibers)

43
Q

What is the characteristic cell of liposarcomas?

A

Lipoblast

Boards Final Review (7 decks)

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