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test > Case 4-6 > Flashcards

Case 4-6 Flashcards

1
Q

What are the layers of the heart wall and what epithelium are they made of ?

A

Endocardium - simple squamous
Myocardium - striated sarcomeres
Epicardium - simple squamous

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2
Q

What is the significance of isovolumetric contraction ?

A

Short time in systole where AV and semilunar valves are shut. Volume constant with pressure ^

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3
Q

Give two examples that would increase after load by ^aortic pressure and systemic vascular resistance

A

Aortic stenosis or ventricle dilation

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4
Q

What substances cause vasoconstriction and vasodilation of the endothelium ?

A

Vasoconstriction; endothelin, vasopressin

Vasodilation; NO, ACh

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5
Q

How do foam cells form during atherosclerotic plaque formation ?

A

Endo dysfunction ^LDL permeability. LDL oxidised in intima, monocytes enter -> macrophages. They bind to LDL -> foam cells ^inflam process , seen as yellow fatty lesions on arterial wall

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6
Q

How does angina arise after foam cell formation ?

A

Collagen deposited forming cap over the plaque, this limits flow (stenosis) -> angina.

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7
Q

What is the difference between stable and unstable angina in terms of plaque rupture /

A

Stable, plaque more fibrous than lipid

Unstable, ^rupture risk lipid rich and inflamed

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8
Q

What is the difference between stable and unstable angina in terms of sx ?

A

Stable, sharp chest pain on exertion relieved by rest or GTN
Unstable, pain comes on at rest.
Both show no troponin increase

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9
Q

How would you manage ACS clinically ?

A

GTN, b blockers (bisoprolol) , CCBs (amlodipine) , Nicorandil (vasodilator) , Ivabradine (rate limiter)

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10
Q

How would you manage ACS acutely ? (MONA)

A

Morphine, O2, Nitrates, aspirin until they can get to a Catheter lab for stenting

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11
Q

Name an anticoagulant medication and reason for use ?

A

Warfarin used at ^risk of clotting events in non vascular trauma causes eg. turbulent blood flow in AF

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12
Q

What is Clopidogrel ?

A

Inhibits platelet P2Y12 ADP receptor that normally triggers platelet activation (post MI)

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13
Q

What drug can be used to dissolve an existing drug ?

A

Fibrinolytic drug eg. Tenectaplase used when thrombus causes ischaemia. Recombinant form to tissue plasminogen activating factor (tPA) which mediates plasminogen to plasmin rapidly dissolving clots by fibrinolysis.

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14
Q

What is the antidote for tenectaplase ?

A

Tranexamic acid

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15
Q

What is the action of Nicorandil ?

A

Vasodilator used in stable angia. Stimulates guanyl cyclase ^cGMP and PKG which decreases Ca and activates KATP efflux -> hyper polarisation

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16
Q

What is the exogenous pathway ?

A

TAGs from gut to liver. Chylomicrons in blood go to peripheral tissues (lipoprotein lipase) break down into TAGs + FFA + glycerol. Chylomicron remnant ApoE binds to liver and endocytosed and hydrolysed in lysosomes again.

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17
Q

Which pathway goes from liver to tissues and what is the first step of packaging ?

A

Endogenous pathway. TAG + cholesterol packaged with apolipoprotein B100 forms VLDL

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18
Q

Where does VLDL go in the endogenous pathway ?

A

in blood meets HDL and matures. in tissue meets lipoprotein lipase -> glycerol/FFA (becomes IDL and HDL). IDL absorbed by liver where lipase removes TAGs -> LDL. LDL binds to tissue via apoB100 on LDL -> lysozyme -> cholesterol

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19
Q

How would a decreased preload affect a PV loop diagram ?

A

Decreases SV and EDV so curve goes down and left

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20
Q

If the curve on a PV loop got taller and thinner what change is likely to have happened ?

A

^afterload ^wall stress, aortic P and R both increase. CO falls as SV falls so width decreases and ESV ^.

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21
Q

How does ^inotropy affect the PV loop ?

A

^SV so ^loop size with decreased ESV. Curve moves left and larger.

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22
Q

What is the difference between the Left and Right lung ?

A

Left has two lobes (sup/inf) divided by oblique fissure

Right has sup/middle/inf divided by horizontal and oblique fissure

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23
Q

What features does the trachea have that make in functional in the conducting airway ?

A

Has goblet cells and cilia. Serous and mucous glands to humidify and trap air

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24
Q

Which bronchus is more prone to aspiration and why ?

A

R bronchus is shorter and straighter so more common. Made of pseduostratified ciliated columnar epithelium with goblet cells.

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25
Q

How do the bronchioles differ from the bronchi ?

A

Bronchioles are simple cuboidal with no cartilage/goblet cells. Lots of SM to control air flow

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26
Q

What are the different cell types in the respiratory bronchioles ?

A

Clara cells produce surfactant
Type 1 alveoli (pneumocytes) useful for diffusion joined by tight junctions
Type 2 round/dark nuclei. Secrete surfactant and are a stem cell precursor for type 1

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27
Q

What is the function of Clara cells ? (5)

A

In terminal bronchioles have microvilli, they secrete glycosaminoglycans which reg hydration and H2O homeostasis. Maintain structure and function, modulate inflammatory response. Influence tissue repair and remodelling.

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28
Q

How is mucous viscosity determined ?

A

Cl moves from serous cells through Ch from interstitial to lumen pulling H2O with it so Cl^ and H2O ^. Important in CF

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29
Q

What is the R to L shunt ?

A

When blood goes straight to LV without being oxygenated due to poor perfusion of the alveoli

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30
Q

How is bronchoconstriction initiated ?

A

PSNS (vagus) ganglia synapse in large airways, contain NTs: ACh, VIP, NOS which innervate SM causing bronchoconstriction and vasodilation ^mucous flow

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31
Q

How is bronchoconstriction reversed ?

A

Atropine (muscular antagonist)

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32
Q

What is the effect of ACh on M1, 2 and 3 receptors ?

A 
M1 = ^preganglionic transmission
M2 = decreases Each 
M3 = ^SM contraction
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33
Q

What is the cough reflex ?

A

receptors/afferent nerves/eff nerves/effector muscles trigger deep inspiration ^intrathoracic P when larynx is closed -> when larnyx opens causes cough

34
Q

What are the afferent nerves, efferent nerves and control centre involved in the cough reflex ?

A

Afferent nerves; CN IX, X
Efferent nerves; vagus, phrenic, spinal motor
Control centre; medulla, Nucleus tractus solitaris.

35
Q

Which area of the lung is the best perfused and ventilated ?

A

The base/ bottom of lung

36
Q

What is the difference between anatomical and physiological dead space ?

A

Anatomical; air in conducting resp tract that doesn’t take part in gas exchange (top of lungs)
Physiological; vol of air in resp zone not part of gas exchange

37
Q

What is the indication if VA:Q = 0 and infinity?

A

0, perfused but not ventilated

Infinity, ventilated not perfused

38
Q

How does smoking ^lung infection risk ?

A

Tobacco ^free radicals which inactive antiproteases and cause tissue damage -> neutrophil/macrophage elastase ^. Air is trapped in the lung and cilia too damaged to move mucous so rate ^

39
Q

What def can worsen a prognosis of lung infection ?

A

alpha 1 AT deficiency

40
Q

What is Cor pulmonale ?

A

RV hypertrophy from pulmonary HT

41
Q

How is breathing controlled voluntarily and involuntarily ?

A

Voluntary; cortex -> spinal cord -> resp muscles.

Involuntary; limbic system/hypothalamus -> pneumotoxic + apneustic centre -> medulla -> spinal cord -> resp muscles

42
Q

What is the difference between peripheral and central chemoreceptors ? (location, response, speed)

A

Peripheral; carotid and aortic bodies , O2 down/^CO2/pH down, rapid response
Central; ventrolateral surface of medulla , pH of CSF, slower

43
Q

Why is O2 contraindicated for COPD ?

A

Decreases the hypoxic drive so px would stop breathing

44
Q

What is the difference between type 1 and 2 respiratory failure ?

A

1 (O2 fails) hypoxaemia with normal/low PCO2; decrease O2 (altitude) , diffusion deficit, VQ mismatch, R/L shunts
2 (ventilation failure) hypoxaemia and hypercapnia; depressed resp centre/muscle weakness, chest wall deformity, severe lung disease (COPD/asthma) , obesity, headache worse in morning

45
Q

How would you tx obstructive sleep apnea ?

A

CPAP, weight loss, reduce alcohol consumption

46
Q

What is compliance and how does it vary with age ?

A

How easily the lungs stretch. decreases in fibrosis, ^with age and emphysema (decreased elastin). Determined by surface tension and lung elasticity

47
Q

What is the the function of surfactant ?

A

Produced by type 2 alveoli and Clara cells. Decreases surface tension so the lungs don’t collapse. Hydrophobic heads immersed in H2O lining of the alveolar wall.

48
Q

What is infant respiratory distress syndrome and what are the sx (3) ?

A

Not enough surfactant in newborn babies leads to lung collapse
Sx; blue discolouration, ^RR, nasal flaring

49
Q

What is asthma and what is the familial risk ?

A

Hyperactive airways -> obstructive disease that’s reversible. Eczema and hay fever common
1 parent = 40% , 2 = 80%

50
Q

What is bronchiectasis, what are the sx (3)and tx (3) ?

A

Chronic inflammation -> permanent dilation of bronchial tree.
Sx; cough, mucous secretion, chest pain.
Tx; airway clearance, mucolytics, inhalers

51
Q

What are the common causes of commonly acquired and hospital acquired pneumonia ?

A

Common; less mortality, strep pneumoniae

Hospital; ^mortality, staph aureus

52
Q

How would you assess pneumoniae and what would be the tx plan ?

A

CURB-65 (confusion, urea, RR, BP, >65)

If >2 give IV abx

53
Q

What is the difference between pleural effusion and pneumothorax ?

A 
effusion = fluid 
Pneumothorax = air
54
Q

What are coal miners pneumoconiosis and pulmonary fibrosis examples of ?

A

Interstitial lung disease

55
Q

How would restrictive and obstructive lung conditions differ in spirometry ?

A

Obstructive (COPD, asthma) <0.7 (long drawn out)

Restrictive >0.7 (both decrease but proportionally)

56
Q

What is the difference between a severe of the fibres between the pons and medulla on resp control ?

A

Pons fine tunes and controls rate so patho causes irregular breathing
Medulla is the main centre so patho causes no breathing.

57
Q

What is the action of the cortex on resp action ?

A

Can override medulla, ^CO2 (holding breath) relays back to centre and forces inhale.

58
Q

What is the flow of CSF up to 4th ventricle ?

A

Choroid plexus (lat ventricle) -> foramen of monro -> 3rd -> aqueduct of sylvias -> 4th

59
Q

What is short term memory ?

A

Small amounts of info for a few seconds. Typically 7 +/- 2 items.

60
Q

What is explicit memory ?

A

Branch of LTM that is open to intentional retrieval (consciousness)

61
Q

How is declarative memory divided ?

A

Facts and events

Episodic (events/experience) and semantic (facts and concepts)

62
Q

What is classical conditioning?

A

Learning procedure, neutral stimulus paired with response provoking stimulus such that stimulus causes response

63
Q

Where is the hippocampus located and what is its function?

A

Medial temporal lobe. Explicit and declarative memory. Involved in creation of new memories

64
Q

Where are stable LTM stored and how are memories consolidated ?

A

Neocortex is the store of ‘remote memory’. Consolidation occurs between hippocampus and neocortex

65
Q

What is anterograde amnesia ?

A

New info problems; encode, store, retrieve failure. Affects hippocampus so new memories can’t be created.

66
Q

Which memory is preserved in anterograde amnesia ?

A

Affects explicit memory not implicit so you can’t learn new facts but you retain the subconscious skills you already have eg. driving.

67
Q

What pathology arises from damage to the neocortex?

A

Retrograde amnesia, problems with memories of past events (can’t store LTM)

68
Q

What are some of the causes of amnesia ? (6)

A

Temporal lobe surgery, herpes simplex encephalitis, anoxia/hypoxia, Korsakoff syndrome (b1 def in alcoholics) , alzheimers (most common but not pure form of amnesia) , vascular dementia

69
Q

How does the volume of the brain change with age, which area is affected the most ?

A

Vol of brain decreases 5% every decade over 40

Frontal lobe shrinks most rapidly.

70
Q

What effect does Alzheimers have on the brain ?

A

Hippocampus normally shrinks slowly but will rapidly shrink if AD.

71
Q

How do the temporal and occipital lobes change with age?

A

They shrink slowly (limited change)

72
Q

What type of memory is affected through ageing ?

A

Fall in episodic memory. Increase in semantic.

73
Q

How do grey and white matter change in ageing ?

A

Grey matter shrinks (neuronal cell death) due to declining synaptic connections so reduced cognitive processing
White matter, myelin shrinks with age so reduced conduction

74
Q

How do the production of DA and 5HT change with age ?

A

Brain generates fewer NTs with ageing so decrease in cognition, memory and ^depression

75
Q

How does Alzheimers affect the brain ?

A

Cortex shrivels so less planning, thinking and memory/ Ventricles fill with CSF grow larger. Hippocampus slowly shrinks

76
Q

Which proteins are involved in Alzheimers ?

A

B amyloid protein extracellular and Tau protein intracellularly

77
Q

What are the sx of Alzheimers ? (4)

A

Gradual onset progressive memory decline, anterograde amnesia key, semantic memory declines, remote memory affected last

78
Q

What are the tx options for AD?

A

Reversible acetylcholinesterase inhbitors; Donepezil, Galantamine, Rivastigmine
NMDA receptor antagonist and nAChR antagonist; Memantime

79
Q

How does vascular dementia differ to AD ? (4)

A

More sudden onset, stepwise coarse. CV hx more important with neuropathy findings; sensory + motor sx, visual problems, EPSEs

80
Q

Which dementia is linked to Parkinsons ?

A

Lewy body dementia. Cognitive fx dominate. Visual hallucinations from early on often of people and animals

81
Q

What is Pick’s disease and where does it affect ?

A

Frontotemporal dementia. Neurodegeneration <65 onset. Strong genetic link. Personality/behavioural changes often key early fx.

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