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Summary questions Flashcards

1
Q

examples of end arteries?

A

coronary arteries
accessory renal arteries
branches of central artery of the retina

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2
Q

what may be seen on examination of a patient’s face with vit B12 deficiency?

A

pallor- pernicious anaemia

angular stomatitis- inflammation at corners of mouth, may also result from Fe or thiamine deficiency

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3
Q

GI causes of clubbing?

A

IBD
cirrhosis
GI lymphoma
malabsorption e.g. celiac disease

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4
Q

Resp causes of clubbing?

A 
cystic fibrosis
lung cancer
COPD
fibrosing alveolitis
sarcoidosis
TB
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5
Q

what may be seen when looking at eyes in wilson’s disease: accumulation of Cu, can cause hepatocellular jaundice?

A

fleischer rings=green-yellow ring at corneal margin

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6
Q

what sign on examination is indicative of cholecystitis?

A

Murphy’s sign: lay 2 fingers over RUQ and ask patient to breathe in, causes pain and arrest of inspiration as inflamed GB impinges on fingers
*Bower’s sign: back pain

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7
Q

signs of dehydrated patient?

A

drying of oral mucosa
loss of skin turgor
sunken eyes

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8
Q

signs on examination of renal artery stenosis patient?

A

renal artery bruits
femoral bruits
weak leg pulses

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9
Q

problem of ACEIs if renal artery stenosis?

A

inhibit angiontenin II’s preferential action on efferent arteriole to constrict it to increase pressure to increase GFR

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10
Q

why would a renal artery stenosis patient experience hypokalaemia?

A

reduced GFR as a result of impaired renal perfusion, which activates RAAS, with aldosterone release from zona glomerulosa of adrenal cortex stimulating Na+ pump synthesis and increased insertion on BL memebrane of cortical CD, and stimulates apical Na+ and K+ channel activity which increase Na+ reabsorption and K+ secretion.

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11
Q

ECG changes of hyperkalaemia?

A

P wave loss
widening QRS complexes
loss of ST segment
tall, wide T waves

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12
Q

ECG changes of hypokalaemia?

A

progressive lengthening of PR interval
ST segment depression
T wave flattening
increase in U wave

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13
Q

symptoms of PE?

A

sharp, pleuritic chest pain
haemoptysis
dyspnoea

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14
Q

characteristics of patient with hypovolaemic shock?

A

tachcardia
cold, clammy extremities
pale skin
weak pulse

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15
Q

characteristics of patient with toxic (septic) shock?

A

tachycardia
strong pulse
warm, red extremities- as vasodilation, BUT in later stages vasoconstriction occurs

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16
Q

characteristics of patient with anaphylactic shock?

A

difficulty breathing
collapsed as impaired perfusion- deecreased a BP
rapid HR and strong pulse- SNS
red, warm extremities- vasodilation

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17
Q

at which 3 sites is BP regulated?

A

kidneys- blood vol regulated by Na+ reabsorption and excretion, altering SV
heart- CO altered by altering rate and force of contraction
vasculature- regulates TPR

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18
Q

non pharmacologic tment of hypertension?

A

weight loss
reduce salt intake
exercise
stop smoking

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19
Q

pharmacologic tment of hypertension?

A 
ACEIs
Ang II receptor blockers
thiazide diuretics
beta blockers
vasodilators
Ca2+ channel blockers
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20
Q

what will happen in the pulmonary circulation in the short term if PA pressure is increased due to compromisation of left heart?

A

pulmonary oedema

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21
Q

clinical manifestations of pulmonary oedema?

A

pink frothy sputum
paroxysmal nocturnal dyspnoea
orthopnoea

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22
Q

what happens to resistance in pulmonary vessels in long term if pulmonary arterial pressure increased?

A

vascular remodelling, so vessels are permanenetly narrowed

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23
Q

characteristics of an exercise stress test?

A

exercise with increasing intensity

exercise until angina occurs, HR altered or ECG changes

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24
Q

characteristics of an exercise stress test?

A

exercise with increasing intensity

exercise until angina occurs/ symptoms of reduced myocardial perfusion, HR altered or ECG changes

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25
Q

what happens to ease of brain perfusion if IC pressure rises, and describe Cushing’s reflex?

A

perfusion reduced

reflex: ischaemia due to reduced perfusion in medullary centres activates sympathetically mediated response to increase mean arterial BP.
* mean arterial BP= 1/3 systolic + 2/3 diastolic

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26
Q

what are amyloidoses?

A

abnormal deposition of insoluble proteins

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27
Q

describe alpha thalassaemias

A

impaired production of alpha chains in Hb. Excess of beta globin chains in adult Hb and excess of gamma chains in newborns. unstable tetramers formed by beta globin subunits, excess gamma globin subunits form tetramers which are poor O2 carriers as affinity for O2 too high so O2 not released to tissues
may be reason for O2 saturation of Hb not being 100% despite being healthy

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28
Q

anaemia that occurs with beta thalassaemias?

A

microcytic anaemia

insufficient Hb to fill rbc as beta globin chains not produced so small rbc

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29
Q

why might a patient with lung cancer have a moon shaped face, purple striae, and central obesity?

A

cushing’s syndrome ( excess cortisol) as a reuslt of ACTH secretion by a small cell carcinoma of the lung

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30
Q

primary and secondary action of nitrates to treat angina

A 
primary= venodilation
secondary= dilation of coronary arteries
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31
Q

where is AngI converted into AngII?

A

lungs

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32
Q

contrast dysplasia, metaplasia and neoplasia

A

metaplasia and dysplasia are reversible. metaplasia refers to the reversible change from 1 differentiated cell type to another differentiated cell type, and the replacement cells are fully differentiated and matured, whereas dysplasia refers to abnormal differentiation and maturation of cells where they show disordered tissue organisation but this is still a reversible change. neoplasia is irreversible and refers to an abnormal proliferation of cells which persists even after the initiating growth stimulus has been removed.

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33
Q

what is pseudohypertrophy and give an example of a disease state in which it occurs?

A

pseudo= false, so pseudohypertrophy refers to something enlarging not as a result of an increase in number or size of the functional elements e.g. muscular pseudohypertrophy- muscles appear larger but this is due to increased fat deposition rather than an increase in muscle proteins, this happens in Duchenne’s muscular dystrophy e.g. of the calf muscles.

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34
Q

where is angiotensinogen produced?

A

liver

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35
Q

what is it it important to examine in patients with hypertension?

A

the optic fundi, as retinopathy occurs with hypertension

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36
Q

common symptom in patients presenting with hypothyroidism?

A

depression

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37
Q

most common cause of hypothyroidism?

A

iodine deficiency

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38
Q

T4 is usually prescribed as what drug for hypothyroidism?

A

levothyroxine

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39
Q

what should a patient be considered to have until proven otherwise if presenting with otorrhoea and hearing loss, and why is this condition a problem in children?

A

cholesteatoma
hearing loss caused may result in a neurological defecit in the child as their learning to speak during development is based on what they hear

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40
Q

why may you be more likely to be a carrier for sickle cell disease if your ancestors are from sub-saharan africa?

A

malaria is endemic here and being a carrier can help protect against malaria

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41
Q

characteristics of the 3 different types of muscle fibres?

A 
skeletal: peripherally positioned nuclei
multinucleated
long and cylindrical fibres
cardiac: centrally positioned nuclei
usually 1 or 2 nuclei per cell
intercalated discs
muscle fibres branch and anastomose
smooth: spindle-shaped
elongated and centrally placed nucleus
sometimes confused with fibroblasts
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42
Q

what would the pulse be like in a patient with hyperkalaemia?

A

fast and irregular- may indicate worry of going into ventricular fibrillation and cardiac arrest

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43
Q

what is pH?

A

pH= kPa+log([HCO3-]/pCo2x0.23)

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44
Q

how is creatine phosphate in skeletal muscle formed for use as a high energy molecule that is readily mobilised?

A

creatine+ATP, which gives creatine phosphate+ADP catalysed by creatine kinase

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45
Q

presenting symptoms of patient with trochlear nerve damage?

A

double vision when walking downstairs (diplopia)

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46
Q

what is the weakest part of the orbit?

A

the medial and inferior walls
medial= ethmoid, lacrimal and maxillae
inferior= maxillae, zygomatic and palatine

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47
Q

what signs may a patient with a blowout fracture have?

A

periorbital ecchymosis
subconjunctival haemorrhage
loss of sensation over upper cheek area

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48
Q

where might orbital contents move into in a blowout fracture?

A

the paranasal sinuses

blood may also be found in sinuses e.g. maxillary

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49
Q

what is oral bioavailability in what is it affected by?

A

proportion of a drug given orally (or any route other than IV) that reaches systemic circulation i nan unchanged form.
Affected by chemical form of drug, administration route and patient-specific factors e.g. GI and hepatic disorders, and enzymes.

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50
Q

amount can be used to measure oral bioavailability, what would amount be affected by?

A

1st pass metabolism and gut absorption

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51
Q

what is the therapeutic ratio?

A

max tolerated dose/min effective dose

LD50/ED50

52
Q

what is LD50 and ED50?

A 
LD50= dose of drug that causes a toxic response in 50% of pop, ED50= drug dose that is therapeutically effective in 50% of pop.
LD50/ED50= therapeutic ratio, larger ratio= greater difference between a dose which is toxic and a dose which is effective.
warfarin= narrow therapeutic index
53
Q

difference between 1st and 0 order kinetics?

A 
1st= rate of drug elimination proportional to dose of drug
0= rate of elimination constant, so only so much can be eliminated per time period no matter what drug dose is
54
Q

what is the worry with using opioids e.g. morphine, for pain relief?

A

can cause respiratory depression which may cause death

55
Q

what is a Pott’s fracture?

A

result of excessive eversion of foot. Pulls on strong medial ligament, often tearing off medial malleolus. Talus then moves laterally, shearing off lateral malleolus or more commonly breaking fibula superior to tibiofibular syndesmosis. If tibia carried anteriorly, post. margin of distal end of tibia is also sheared off by talus, so trimalleolar fracture.

56
Q

why might a patient lose sensation over the medial border of their foot in a saphenous cutdown?

A

in trying to access the great saphenous vein, the saphenous nerve may be damaged, which innervates the medial border of the foot

57
Q

which structures occupy the tarsal tunnel located posterior to medial malleolous and formed on the outside by the flexor retinaculum?

A

TDAVNH
tendon of tibialis posterior, flexor digitorum longus, posterior tibial artery, posterior tibial vein, tibial nerve, flexor hallucis longus

58
Q

which criteria are used when trying to decide if their is a causal relationship between two variables?

A

Bradford-Hill criteria
Strength, specificity and consistency of association
reversibility, temporal sequence, dose-response relationship, coherence of theory
biological mechanism, analogy

59
Q

why might the retinoblastoma gene be involved in the development of some cancers?

A

it is a tumour suppressor gene so mutations in the gene may result in the loss of the protein’s function to suppress cell growth by inhibiting progression through the cell cycle due to its action at the restriction point of the cell cycle

60
Q

drugs used in the tment of angina?

A 
nitrates e.g. GTN spray
beta blockers
Ca2+ blockers
ACE inhibitors
aspirin- anti-platelet
statin
61
Q

most common causative organism for a sore throat?

A

Group A streptococci (strep throat!)

62
Q

examples of drugs which have 0 order kinetics?

A 
warfarin
aspirin
phenytoin- used in epilepsy
alcohol
theophylline- xanthine drug, can be used in asthma
tolbutamide
63
Q

what is tolbutamide used in the treatment of?

A

type 2 diabetes

64
Q

name given to upward projection of ethmoid bone to which falx cerebri attaches?

A

crista galli

65
Q

through what do olfactory nerve fibres travel through to reach the nasal cavity?

A

multiple small foramina in cribiform plate of ethmoid bone

66
Q

from which artery do the ethmoidal arteries arise from?

A

the opthalmic- branch of the ICA

67
Q

3 bones comprising anterior cranial fossa?

A

frontal, ethmoid and sphenoid

68
Q

3 bones comprising middle cranial fossa?

A

sphenoid and the 2 temporal

69
Q

important structures located in middle cranial fossa?

A

pituitary gland, and the temporal lobes of the brain

70
Q

complications of pituitary surgery?

A

haemorrhage, diabetes insipidus, visual disturbances, meningitis and CSF rhinorrhoea

71
Q

the most perfused organs in the normal state are the kidneys, the brain and the skin, therefore what 3 things can be checked to assess hypovolaemia in a patient who may go into shock?

A

urine output
glasgow coma scale
capillary refill

72
Q

distinguish between dysphonia, dysarthria, dysphasia and dysphagia?

A

dysphonia- disorders of the voice, problem with producing vocal sounds
dysarthria- problems with speech making the pronunciation of words difficult
dysphasia- problem with language so difficult to communicate
dysphagia- difficulty swallowing

73
Q

2 things which normally prevent neoplasia in the body?

A

apoptosis

DNA repair

74
Q

apoptosome constituents?

A

cytochrome C
APAF1
caspase 9

75
Q

serious problems which may result from a benign tumour?

A

obstruction to fluid flow e.g. epithelial tumour blocking a duct
pressure on adjacent tissue e.g. meningeal tumour can cause epilepsy
hormone producing
transform to malignant
anxiety

76
Q

common sites of dysplasia?

A

stomach, bladder, cervix

77
Q

difference between an in-situ and invasive malignancy?

A

in-situ has not invaded through the epithelial basement membrane

78
Q

why are most cancers carcinomas?

A

as epithelial cells proliferating the most

79
Q

contrast routes of metastasis for carcinomas and sarcomas?

A

carcinomas prefer lymph

sarcomas prefer blood

80
Q

what is myeloma?

A

malignant neoplasm of plasma cells (antibody producing cells formed from B lymphocytes), results in presence of abnormal Igs in the blood
Bence-Jones proteins found in urine in multiple myeloma patient, these are the light chain part of the monoclonal antibodies produced in the disease

81
Q

example of an oncogene associated with lung and colon cancer?

A

Ras

82
Q

viruses that can cause cancer?

A

epstein-barr= burkitt’s lymphoma
HPV= cervical carcinoma
Hep B= hepatocellular carcinoma

83
Q

examples in the body of where smooth muscle is found?

A

myometrium of the uterus
bladder
blood vessels
ciliary muscles

84
Q

to what carpal bones does the flexor retinaculum attach? *

A

proximally to the scaphoid and trapezium

distally to the pisiform and hamate

85
Q

structures which pass through the carpal tunnel? *

A

4 tendons of flexor digitorum superficialis
4 tendons of flexor digitorum profundus
tendon of flexor pollicis longus
median nerve

86
Q

inheritence pattern of sickle cell anaemia and CF? what are the features of this inheritence pattern?

A

autosomal recessive
skips generations
male and females equally affected
both parents must at least be carriers for the disease to be inherited

87
Q

give 4 causes of poor regional perfusion?

A

arterial occlusion: PAD and CAD

venous congestion: DVT and varicose veins

88
Q

why is the leg subject to ulcer formation in a patient with varicose veins?

A

blood stasis in superficial veins as unable to drain effectively into deep veins, so this means a lack of blood flow to particular areas of the leg so the skin is poorly nourished which means even minor trauma can causes ulcers to form.

89
Q

how do the calves appear in a patient with a DVT?

A

tender, swollen, red and painful

risk of PE= dyspnoea and chest pain- sharp and pleuritic

90
Q

why might a patient with coronary artery disease experience chest pain on exercise but be fine at rest?

A

With exercise, myocardial O2 demand increased, but diastole shortened with increase in HR so reduced filling time for coronary arteries, so insufficient blood able to be provided to the myocardium producing ischaemia which stimulates pain fibres.

91
Q

ECG findings for ischaemic heart disease?

A

Often normal at rest but may be ST depression as abnormal spread of depolarisation.
may also be T wave inversion
Must do an exercise stress test where patient exercises with increasing intensity (usually on a treadmill) until desired HR reached, ECG changes noted or chest pain occurs. ECG, HR and BP monitored. +VE test if chest discomfort or ECG changes.

92
Q

causes of conductive hearing loss?

A 
glue ear (chronic otitis media with effusion?)
acute otitis media
perforated TM
too much ear wax
otosclerosis
cholesteatoma
93
Q

causes of sensorineural hearing loss?

A 
menieres disease
acoustic neuroma
viral infection of vestibulcochlear nerve e.g. mumps or rubella
meningitis
MS
stroke
94
Q

which ion channel is defective in patients with CF?

A

CFTR channel= cystic fibrosis transmembrane conductance regulator channel, found on the surface of epithelial cells e.g. in the lungs and the pancreas.

95
Q

why are Ca2+ channel antagonists used in the tment of angina?

A

act on peripheral arterioles to result in relaxation which causes a decreased TPR so reduced afterload on the heart.
also reduces force of contraction of the heart (-ve inotropic effect), so reduce workload and hence myocardial O2 demand.

96
Q

3 classes of acute coronary syndromes?

A

unstable angina
NSTEMI
STEMI

97
Q

How does unstable angina occur and what are its features?

A

atherosclerotic plaque disrupted and thrombus formation partially cuts off blood supply to the myocardium making its O2 demand difficult to meet even at rest, but obstruction to b.supply is of a limite duration and extent.
ECG: may be ST depression and/or T wave inversion
no detectable necrosis so no raised troponin or cardiac enzymes as PMs of myocardial cells intact.
Rapid onset chest pain at rest, severe central- radiates less.

98
Q

why do patients present with pallor when suffering an MI?

A

peripheral vasoconstriction occurs due to strong SNS activation

99
Q

what happens in a coronary artery to cause an MI?

A

atheromatous plaque ruptures forming a thrombus which detaches or propagates along artery and blocks it, stopping blood from reaching the mycoardium so necrosis ensures.

100
Q

contrast STEMI with NSTEMI?

A 
STEMI= necrosis is of full thickness of the myocardial wall
NSTEMI= more limited- ST depression and inverted T waves.
101
Q

why does a downward Q wave occur with STEMIs?

A

electrode is now viewing the back of the heart due to death of mycoardial tissue so rather than seeing an upward R wave, it sees a downward Q wave as depolarisation is moving away from the viewing lead.

102
Q

why does VF causes cardiac output to plummet?

A

uncoordianated electrical activity causes uncoordinated contraction of myocardium

103
Q

Adrenaline may be given to a patient suffering cardiac arrest. What is the importance of its effect on TPR?

A

it increases it by causing peripheral arteriolar constriction necessary to elevate BP so can get good perfusion of body with blood.

104
Q

what is thought to be the reason as to why malignant melanoma commonly metastasises to the brain?

A

due to neural crest cell origin of melanocytes

neural crest cells= ectodermal cells found along the border of the neural tube during development

105
Q

which cells of the medulla increase HCO3- release in response to continually high pCO2 in a COPD patient?

A

choroid plexus cells

106
Q

name the deep extensor muscles of the forearm

A 
extensor indicis
abductor pollicis longus
extensor pollicis longus
extensor pollicis brevis
supinator
107
Q

name a drug that is a dopamine agonist and so can be used to treat hyperprolactinaemia by inhibiting prolactin release from the anterior pituitary

A

bromocriptine

108
Q

why does a HF patient feel breathless?

A

blood unable to be pumped effectively out of the heart so accumulates in the chambers, increasing the pressure. This pressure backs up into the pulmonary circulation, so increased hydrostatic pressure in pulmonary capillaries which forces fluid out into the pulmonary interstitium, causing pulmonary oedema- lengthens the diffusion distance so oxygenation of the blood is made more difficult, cause of type 1 resp. failure.

109
Q

where are central chemoreceptors found?

A

medulla

110
Q

why does cor pulmonale occur with chronic resp failure?

A

hypoxia- hypoxic pulmonary vasoconstriction causing pulmonary hypertension and subsequent RHF, resulting in systemic oedema as pressure backs up into venous sytstem.

111
Q

why is increased 2,3-BPG useful in chronic hypoxia?

A

binds to Hb to promote its low affinity T state so O2 more readily released to the tissues.

112
Q

why is an IV infusion of a Na+ rich fluid used in fluid resuscitation?

A

want to expand plasma volume to increase BP and hence maintain organ perfusion, so want fluid to remain in ECF rather than travel into ICF (which you would want if given IV fluid for routine maintenance), and Na+ can’t pass from interstitial fluid into cells so fluid stays in ECF.
examples e.g. Hartmann’s solution or sodium lactate.

113
Q

3 reasons why IV fluid may be needed?

A

resuscitation e.g. SHOCK
routine maintenance
replacement

114
Q

2 main differences between bronchi and bronchioles?

A 
bronchi= crescenteric plates of cartilage in walls, cartilage absent from bronchioles
bronchi= submucosal glands e.g. mucous glands, these are absent in bronchioles
115
Q

importance of basement membrane when thinking about tumours?

A

benign= never cross BM, insitu= haven’t yet crossed BM e.g. carcinoma in situ, malignant- prenetrate BM

  • *malignant melanoma- good prognosis indicated by melanocytes being retained above the basement membrane as melanocytes normally occupy the stratum basale lying above the BM.
  • *AI destruction of melanocytes chatacterises Vitiligo- reduced pigmentation of skin, often symmetrical pattern- possbily related to NS control due to neural crest cell origin of melanocytes.
116
Q

potentially premalignant transformation of cervical cells detected by cervical cancer screening?

A

cervical intraepithelial neoplasia

117
Q

what happens in psoriasis?

A

excessive skin flaking following extreme proliferation of epidermal basal layer, leading to gross thickening of stratum spinosum and production of excessive stratum corneum cells.

118
Q

3 major airway changes in COPD?

A

loss of ciliated cells
goblet cell hyperplasia
submucosal mucous gland hypertrophy, causing excessive mucus secretion

119
Q

RFs for Barrett’s oesophagus?

A

smoker
increasing age (50-70)
overweight
long-standing GORD

120
Q

main mechanism by which microvascular complication come about in diabetes mellitus?

A

ROS damage of cells= oxidative stresses and osmotic stresses
structures damaged= glucose dependent- continue to take up glucose even if already have lots, conversion to sorbitol consumes NADPH so lose protection against ROS, and glucose=high osmotic load.
* contrast to macrovascular=atheroma formation as glucose glycosylates proteins in arterial walls, causing endothelial cell dysfunction.

121
Q

enzyme necessary for ketone body production?

A

HMG CoA lyase

122
Q

enzyme necessary for cholesterol production by liver?

A

HMG CoA reductase

123
Q

why does a cancer patient experience cachexia (wasting- muscle loss, fatigue, weakness)?

A

increased catabolism as increased cell proliferation**

124
Q

only part of the pancreas which is intra-peritoneal?

A

tail

125
Q

what is a picomol in mol?

A

10^-12 mol

ESA Revision (15 decks)

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