Pathophysio Flashcards

1
Q

What are the 3 ways to manage acute ischemia? (ST elevation seen)

What about those patients with no symptoms (no ST elevation)?

A
  • Acute perfusion therapy
  • Percutaneous Coronary Intervention (PCI)
  • Thrombolysis

No symptoms:
Use antiplatelet drugs

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2
Q

What are the cells in Islets of Langerhans and what do they produce?

A

𝛃 cells produce insulin, proinsulin
𝞪 cells produce glucagon
δ cells products somatostatin
F cells produce pancreatic polypeptide

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3
Q

Differentiate Type I and Type II diabetes.

A

(ans found on paper)

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4
Q

Describe the complications of DM (acute & chronic) + others

A

(ans found in doc)

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5
Q

Target organs of growth hormone and thyroid hormone?

A

GH- Liver

TH- Thyroid gland

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6
Q

Causes of hypothyroidism

A
  1. Goitre due to iodine deficiency in diet
  2. Hashimoto’s thyroiditis
  3. Removal of thyroid gland
  4. Damage and inflammation of hypothalamus
  5. Use of radioactive iodine for therapeutic purposes
  6. Unfavourable environmental factors
  7. Drug therapy depressing thyroid function
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7
Q

Treatment of hypothyroidism

A

T4 replacement: synthetic version of the T4 called levothyroxine

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8
Q

Causes of hyperthyroidism

A
  1. Diffuse toxic goitre aka. Grave’s disease
  2. Toxic multinodular goitre
  3. Hypersecretion of TSH (secondary)
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9
Q

Treatment of Grave’s disease

A
  1. Drug therapy – (anti hormone) Propylthiouracil, Methimazole
  2. Radioactive iodine therapy
  3. Surgery– Thyroidectomy
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10
Q

State T4 and TSH (and/or TRH) levels in the pri & sec hypothyroidism and hyperthyroidism.

A

Pri hypo: Low T4, high TSH
Sec hypo: Low T4, low TSH

Pri hyper: High T4, low TSH
Sec hyper (non-thyroidal) : High TSH, High TRH
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11
Q

Describe how hypocalcemia is controlled.

A

(found on paper)

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12
Q

Causes of hypoparathyroidism

and its treatment

A
  • Thyroidectomy (Parathyroid gland trauma or removal)
  • ↓ serum Ca and ↑ serum phosphate

Treatment: Calcium/ vitamin D replacement

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13
Q

Causes of hyperparathyroidism and its treatment

A

Pri:
-Parathyroid glands tumors
- ↑ PTH, ↑ serum Ca- hypercalcemia
Treatment: Parathyroid removal

Sec:
- Triggered due to low level of serum Ca
-↑ PTH, in response to ↓ serum Ca
- Renal failure
- Intestinal malabsorption
- Vitamin D insufficiency
Treatment:Pituitary surgery

Tertiary:
Autonomous parathyroid hyperplasia– background of prolonged secondary hyperparathyroidism

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14
Q

State PTH and serum calcium levels in the pri & sec hyperparathyroidism.

A

Pri:
High PTH, high serum calcium

Sec:
High PTH, low or normal serum calcium

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15
Q

What is pulmonary function test?

A

Measures lung volume, capacity, rates of flow and gas exchange eg. spirometry

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16
Q

List some characteristics of chronic bronchitis. (at least 8 out of 12)

A
  • Inhaled irritants → chronic excessive mucus
  • Inflamed & fibrosed lower respiratory passageways
  • Obstructed airways
  • Impaired lung ventilation & gas exchange
  • Dyspnea on exertion
  • Increased sputum production
  • Chronic cough
  • Edema or hypervolemia can be present
  • Hypertrophy & hyperplasia of the bronchial mucous glands
  • Increased goblet cells
  • Ciliary damage
  • Squamous metaplasia of columnar epithelium
17
Q

Test findings of chronic bronchitis

A
  • Chest X-ray may show hyperinflation and increased bronchovascular markings
  • Pulmonary function tests: RV ↑; VC & FEV ↓
  • ABG (Arterial blood gas) analysis reveals ↓ PaO2 and normal or increased PaCO2
  • FBC shows hematocrit (RBCs proportion) over 50% polycythemia (an increase in the number of red blood cells in the body–may lead to issues like blood clot).
18
Q

List some characteristics of emphysema. (at least 6 out of 10)

A
  • SOB/dyspnea
  • Permanent enlargement of alveoli
  • Destruction of alveolar walls and capillary beds
  • ↓ lung elasticity
  • Hyperinflation of lungs → flattened diaphragm → ↓ ventilation efficiency
  • Hyperinflation → ↑ total lung capacity
  • Etiologies: cigarette smoking, air pollution, alpha-1 antitrypsin deficiency
  • Barrel chest
  • Clubbing
  • ↓ breath sounds and ↓ tactile fremitus
19
Q

Test findings of emphysema

A
  • Reveal flattened diaphragm, reduced vascular markings at the periphery, over aeration of the lungs, large retrosternal air space
  • Pulmonary function tests show ↑ RV and TLC
  • ABGs show ↓ PaO2 and normal PaCO2 until later in the disease process
  • FBC– ↑ haemoglobin and hematocrit late in the disease
20
Q

Management of COPD

A
  1. Smoking cessation
  2. O2 therapy
3. Medications:
Beta agonists
Anticholinergics
Glucocorticoids
Theophylline
Phosphodiesterase-4 (PDE-4) inhibitors
21
Q

Causes of pneumonia

A

Caused by infectious agents:

  • Inhalation of contaminants: virus , mycoplasma
  • Contamination from the systemic circulation

Caused by non-infectious agents:
- Aspiration of oropharyngeal secretions composed of normal bacterial flora or gastric contents (25%-35%)

22
Q

Management of pulmonary tuberculosis (TB)

A
  • Tuberculin skin test
  • Chest x-ray :
    Nodules with infiltrates in apex and posterior segments
  • Sputum culture:
    3 consecutive, morning specimens
  • Anti-tuberculosis medications:
    Isoniazid, rifampicin, pyrazinamide, ethambutol
  • Patient education
23
Q

List characteristics of asthma.

A
  • Characterised by coughing, dyspnea, wheezing & chest tightness
  • Narrowing of airways caused by bronchospasm, oedema, mucus plugging
  • Hyper-resonance (sounds that occurs in chest as a result of overinflation of the lung)
  • Use of accessory muscles
  • Pulsus paradoxus (a fall of systolic blood pressure of >10 mmHg during the inspiratory phase.)
24
Q

Test findings of asthma

A

1) Lung function test: ↓ FEV1, & FEV1-FVC ratio & PEFR

2) ABG: pH ↓ , ↑ pCO2

25
Q

Management of asthma

A
  • Control of factors that trigger asthmatic attacks: prevention of exposure to irritants and allergens (Desensitisation)
  • Pharmacologic management :
    1) Controllers: inhaled corticosteroids, long-acting beta 2 agonists, leukotriene modifiers
    2) Relievers: rapid-acting beta 2 agonists, anticholinergics, theophylline
26
Q

Functions of insulin

A

(When blood glucose is high)

  • Promotes glucose uptake by target cells and provides for glucose storage as glycogen
  • Prevents fat and glycogen breakdown
  • Inhibits gluconeogenesis and increases protein synthesis