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EXAM > Clinical Phys 2 > Flashcards

Clinical Phys 2 Flashcards

1
Q

Leptin induces satiety (key role in regulating body weight)
where is it produced?
where does it act?
what does it stimulate?

A
  • produced by adipose tissue (obesity = high leptin levels)
  • acts on satiety centres in HYPOTHALAMUS and decreases appetite
  • stimulates MSH (melanocyte) & CRH (corticotrophin-releasing)
  • low leptin levels stimulate release of NPY (neuropeptide Y)
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2
Q

Ghrelin stimulates hunger
where is it produced?
- levels inc before, & fall after, meals

A

mainly by P/D1 cells lining stomach fundus & epsilon cells of pancreas

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3
Q

Which patients are at higher risk of hyponatraemic encephalopathy?

A

paediatric pts - most noted when they receive hyPOtonic IV fluids e.g. 0.45% NaCl

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4
Q

4 functions of vitamin C

A
  • antioxidant
  • collagen synthesis (cofactor in hydroxylation of proline & lysine)
  • facilitates iron absorption
  • cofactor for norepinephrine synthesis
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5
Q

Features of vitamin C deficiency

A
  • leads to defective collagen synthesis resulting in capillary fragility & poor wound healing
  • gingivitis, loose teeth, general malaise
  • bleeding tendency: gums, epistaxis, haematuria
  • poor wound healing
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6
Q

What are the water-soluble vitamins?

A

B vitamins & vitamin C

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7
Q

What are the fat-soluble vitamins?

A

A, D, E & K

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8
Q

2 factors which increase pulse pressure

A
  • less compliant aorta (age)

- increased stroke volume

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9
Q

Cardiac action potential phase 0 & mechanism

A

Rapid depolarisation

- rapid Na influx (channels automatically deactivate after a few ms)

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10
Q

Cardiac action potential phase 1 & mechanism

A

Early repolarisation

- K efflux

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11
Q

Cardiac action potential phase 2 & mechanism

A

Plateau

- slow Ca++ influx

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12
Q

Cardiac action potential phase 3 & mechanism

A

Final repolarisation

- K efflux

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13
Q

Cardiac action potential phase 4 & mechanism

A

Restoration of ionic concentrations

  • Na/K/ATPase restores resting potential
  • slow Na influx decreases potential difference until the threshold potential is reached -> triggering a new AP
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14
Q

Where is growth hormone secreted?

A

By somatotroph cells of anterior lobe of pituitary gland

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15
Q

2 main functions of growth hormone?

A
  1. postnatal growth & development

2. involved in protein, carbohydrate & fat metabolism (inc increasing lipless & gluconeogenesis)

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16
Q

Mechanisms of action of growth hormone?

A
  • Directly on tissues
  • Indirectly via IGF-1 (secreted mainly by liver)
  • binds to a transmembrane R for growth factor -> receptor dimerization
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17
Q

Factors which increase secretion of GH?

A
  1. GHRH (release in pulses by hypothalamus)

2. fasting, exercise, sleep

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18
Q

2 factors which decrease secretion of GH?

A
  1. glucose

2. somatostatin (somatomedins, circulating IGFs, IGF-1, IGF-2 increase this)

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19
Q

3 subunit proteins of troponin and what do they bind to?

A

Trop C - binds to Ca++ ions to activate muscle contraction (released in both skeletal & cardiac muscle damage therefore poor specificity for myocardial necrosis)
Trop T - binds to tropomyosin forming trop-tropomyosin complex (specific for myocardial necrosis)
Trop I - binds to actin to hold the above complex in place (also specific)

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20
Q

Response & examples of ligand-gated ion channel R’s

A
  • fast response

- nicotinic Ach, Gaba-A, Gaba-C, glutamate

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21
Q

2 types of tyrosine kinase R’s

A
  1. intrinsic TK: insulin, IGF, EGF

2. receptor-ass TK: GH, prolactin, IFN, IL

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22
Q

Feature & examples of guanylate cyclase R’s

A
  • contain intrinsic enzyme activity

- e.g. atrial natriuretic factor, BNP

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23
Q

Response of G protein-coupled R’s?

  • domains?
  • 3 main subunits?
A
  • slow transmission, metabolic processes; activated by wide variety of extracellular signals e.g. peptide hormones, biogenic amines, lipophilis hormones, light
  • 7-helix membrane-spanning domains
  • alpha, beta, gamma subunits
  • named according to alpha subunit
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24
Q

Activation of alpha subunit of G protein-coupled receptors

A
  • ligand binding causes conformational changes to receptor -> GDP is phosphorylated to GTP -> activating alpha subunit
25
Q

Mechanism of Gs

A

Stimulated adenylate cyclase -> inc cAMP -> activates protein kinase A
- e.g. beta 1 & 2, H2, D1, V2 & R’s for ACTH, LH, FSH, glucagon, PTH, calcitonin, PGs

26
Q

Mechanism of Gi

A

Inhibits adenylate cyclase -> decreases cAMP -> inhibits protein kinase A
- e.g. M2 (Ach), alpha-2, D2, Gaba-B

27
Q

Mechanism of Gq

A

Activates phospholipase C -> splits PIP2 to IP3 + DAG -> activates protein kinase C
- e.g. alpha-1, H1, V1, M1, M3

28
Q

Features of hypocalcaemia?

neuromuscular excitability

A
  1. tetany: muscle twitch, cramp, spasm
  2. perioral paraesthesia
  3. prolonged QT interval
  4. chronic: depression, cataracts
29
Q

What is Trousseau’s sign?

A

Carpal spasm when brachial artery is occluded (e.g. by inflating BP cuff & maintaining pressure above systolic) in hypocalcaemia
- more sensitive & specific than Chvostek’s sign

30
Q

What is Chvostek’s sign

A

Tapping over parotid causes facial muscles to twitch in hypocalcaemia

31
Q

Causes of pseudohyponatraemia

A
  • hyperlipidaemia (inc in serum volume)

- venepuncture from drip arm

32
Q

Causes & fluid status in hyponatraemia when urinary sodium > 20

A

hypovolaemia: Na depletion, renal loss
- diuretics, Addison’s, diuretic stage of renal failure
euvolaemia: SIADH, hypothyroid

33
Q

Causes & fluid status in hyponatraemia when urinary sodium < 20

A

hypovolaemia: D&V, sweating, burns, rectum adenoma
hypervolaemia/oedematous:
- 2ry hyperaldosteronism - heart failure, cirrhosis
- reduced gfr i.e. renal failure
- IV dextrose, psychogenic polydipsia

34
Q

Calculate cerebral perfusion pressure

A

CPP = MAP - ICP

35
Q

What is the Cushing reflex?

A

physiological response to increased intracranial pressure -> hypertension + bradycardia (baroRs)

36
Q

Clinical Dx of familial hypercholesterolaemia

  • Chol levels
  • definite FH
  • possible FH
  • Management?
A
  • Adult TC >7.5, LDL-C > 4.9
  • children TC > 6.7, LDL-C > 4.0
  • definite: tendon xanthoma in pts or 1st/2nd degree relatives or DNA-based evidence of FH
  • possible: FHx MI <50yrs in 2nd degree, or <60yrs in 1st degree, or FHx of raised cholesterol levels
  • Rx: specialist lipid clinic referral, maximum dose potent statins, screening to those <10yrs if parent affected. Discontinue statin in women 3/12 before conception (congenital defects risk)
37
Q

How is nitric oxide formed?
What is it’s half-life?
What is present in macrophages?

A
  • from L-arginine & oxygen by NOS: nitric oxide synthetase
  • v short t1/2 of seconds, being inactivated by oxygen free radicals
  • inducible form of NOS in macrophages
38
Q

3 effects of nitric oxide?

A
  1. vasodilation (mainly venodilation)
  2. inhibits platelet aggregation
  3. acts on gauntlet cyclase -> raised intracellular cGMP -> decreasing Ca2+ levels
39
Q

3 causes of hypercholesterolaemia

A

nephrotic syndrome
hypothyroidism
cholestasis

40
Q

Causes of predominantly hypertriglyceridaemia

A

DM, obesity, etoh, liver disease, chronic renal failure

drugs: thiazides, non-selective beta-blockers, unopposed oestrogen

41
Q

What pulmonary surfactant a mixture of?
What is the main functioning component?
When is it first detectable?

A
  • mix of phospholipids, carbs & proteins, released by type 2 pneumocytes
  • DPPC: dipalmitoyl phosphatidylcholine is main component, which reduces alveolar tension
  • 1st detectable c. 28 wks
42
Q

How does pulmonary surfactant work?

A
  1. as alveoli decrease in size, surfactant concentration is increased, helping prevent alveoli from collapsing
  2. it reduces the muscular force needed to expand the lungs i.e. decreases work of breathing
  3. lowers elastic recoil at low lung volumes therefore helps to prevent alveoli from collapsing at end of each expiration
43
Q

What is vitamin B2 (riboflavin)>

What is a sign of deficiency?

A
  • cofactor of flavin adenine dinucleotide (FAD) & flavin mononucleotide (FMN), important in energy metabolism
  • angular cheilitis
44
Q

Haematuria with dysmorphic RBCs found on urine microscopy - where is the haematuria likely to be coming from?

A

Glomeruli origin

45
Q

Ass. conditions of red cell casts in urine?

A

glomerulonephritis

renal ischaemia & infarction

46
Q

Ass. conditions of white cell casts in urine?

A

acute pyelonephritis

interstitial nephritis

47
Q

Ass. condition of granular ‘muddy-brown’ casts in urine?

A

acute tubular necrosis

48
Q

Ass. conditions of hyaline casts in urine?

A

common, non-specific

can be seen after exercise/dehydration

49
Q

Ass. conditions of epithelial casts in urine?

A

acute tubular necrosis

50
Q

Ass. conditions of waxy casts in urine?

A

advanced CKD

51
Q

Ass. conditions of fatty casts in urine?

A

nephrotic syndrome

52
Q

Type of collagen found in bone, skin & tendon, ass with osteogenesis imperfecta?

A

type I

53
Q

Type of collagen found in hyaline cartilage & vitreous humour?

A

type II

54
Q

Type of collagen found in reticular fibre & granulation tissue? (also implicated in vascular variant of Ehlers-Dalos syndrome)

A

type III

55
Q

Type of collagen found in basal lamina, lens & basement membrane. Implicated in aport syndrome & Goodpasture’s syndrome?

A

type IV

56
Q

Type of collagen found in most interstitial tissue & placental tissue; affected in classical variant of Ehlers-Dalos syndrome?

A

type V

57
Q

Tissues with increased levels of flexibility have increased levels of which type of collagen?

A

type III

58
Q

What produces collagen?

- commonest subtype?

A

fibroblasts

type I

59
Q

Inflammatory markers

  • when is CRP useful
  • what makes plasma viscosity superior to ESR?
A
  • CRP useful for detecting bacterial infections
  • Plasma viscosity is unaffected by anaemia/polycythaemia, delays between sample & measurement, and results are independent of age & sex

EXAM (21 decks)

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