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RBF > Stuff to go over before exam > Flashcards

Stuff to go over before exam Flashcards

1
Q

What secretes angiotensin

  • what is absorbed more in kidney due to angiotenisn 2
  • what happens to produce renin
A
  • Liver secretes angiotnesin
  • tubular na, cl, k reabsorption, h20 retention
  • Arteriolar vasoconsticiton - increase BP
  • REnin - deu to decrease pressure in afferent arteriols
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2
Q

Effects of systemic baroreceptors

A
  • These have a thershold - dont work below or above a specific presure - stays the same - dont get a change in pressure
  • saturation - will cause no futhter effect
  • NO and prostacyclin can increase baroreceptor sensitivity
    1. sympathetic outflwo to heart and vessles, reduce cardiac vagal activity, increase catecholmine secretion by adrenal medulla , also get responses to adh and angiotensin 2
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3
Q

COPD

A

-get inflammation in lungs - poorer oxygen perfusion

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4
Q

Criteria to diagnose diabetic ketoacidosis

A
  • hyperglycaemia
  • low bicarb
  • ketonuria
  • low pH
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5
Q

How does insulin effect K?

A

-insulin will stimulate Na/K atpase pump and get more K uptake into cells

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6
Q

How does aldosterone effect K?

A
  1. increase K uptake by cells

2. increases potassium secretion from kidney vis Na/K atpase pump, and get more Na absorbed

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7
Q

Diabetes insipidis

A

renal resistance to adh

so cannot get absorbed water as much

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8
Q

Addisons disease

A
  • pituitary problem
  • low cortisol and aldosterone
  • get hypovolemia and hypotension and high serum K during sever stress e.g acute gastroenteritis, major trauma ect.
  • get high acth and get more tanned due to increase melatonin secretion
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9
Q

Spinal cord levels responsible for resp muscles?

A

anterior horn cells, major resp muscles - the spinal cord would be C3,4,5

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10
Q

Equation for A-a gradient

A

A-a gradient = 20- Pac0/0.8 - Pa02

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11
Q

3 reasons causing bad diffusion

A
  • gas
  • diffusion distance/thickness
  • surface area
  • haemoglobin
  • capillary volume

-alveolar capillary block (increase fibrous tissue due to aspestos - thickened walls)
-loss of diffusing surface - emphysema
-Capillary volume / haemoglobin
pulmonary capillaries e.g if someone has pulmonary hypertension or embolism then will have abnormal diffusion thing, anaemia

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12
Q

what is dead space, and what is a shunt?

A
  • Dead space is when there is no perfusion so get very low V/Q
  • when there is a trapped alveolar, then cannot get ventilation, and have a shunt
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13
Q

wheeze on expiration in asthma + a stridor on inspiration in extrathoracic obstruction.

A

Stridor is an extrathoracic obstruction, can be due to something like croup. What happens is that normally during inspiration negative pressure is generated in the airways which results in an increased tendency for the airway to collapse, given the extrathoracic pressure placed on the airway this causes airway obstruction during inspiratory phase, increased turbulence and therefore the sound of stridor heard. Expiration is passive and airway pressure is not negative therefore the tendency for the airway to collapse is reduced and no sound is heard on expiration

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14
Q

wheeze on expiration in asthma + a stridor on inspiration in extrathoracic obstruction.

A

Stridor is an extrathoracic obstruction, can be due to something like croup. What happens is that normally during inspiration negative pressure is generated in the airways which results in an increased tendency for the airway to collapse, given the extrathoracic pressure placed on the airway this causes airway obstruction during inspiratory phase, increased turbulence and therefore the sound of stridor heard. Expiration is passive and airway pressure is not negative therefore the tendency for the airway to collapse is reduced and no sound is heard on expiration

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15
Q

What is the cause of itching in chronic cholestasis

A

-if have chronci cholestasis, then will most likely have jaundice as there is prolonged bloackage of bile, which will increase amount of biliribun in the blood causing juandice
-this iwll cause itchiness of the skin
-when bile salts get into the skin - they cause itchiness
primary biliary cirrhosis, primary sclerosing cholangitis, obstructive choledocholithiasis, carcinoma of the bile duct, cholestasis (also see drug-induced pruritus), and chronic hepatitis C viral infection and other forms of viral hepatitis

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16
Q

What happens to the body when you have jaundice

A
  • increase billirubin in the body can lead to some problems

- e.g can get toxicity, and get it in brain which causes confusion, tiredness and concentration

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17
Q

What does lactulose do?

A

normally used to treat constipation, however it can be used to reduce the amount of ammonia in the blood and excrete it- resolve confusion ec.t

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18
Q

PBC and PSC

A

Primary bilary cirrhosis autoimmune attack of bile cells in liver, bile can leak into blood and damage liver cells (intrahepatic)

  • can cause cholestasis, obstructive jaundice
  • can get jaundice
  • also can get increase cholesterol
  • can get itchy skin - early itchiness before jaundice
  • get GGT and ALP increase because these are in bile duct cels, and then can also get liver damage due to this
  • AMA antibody positve

Primary sclerosisng cholangitis

  • hardening of tissue of extrahepatic ducts and intra hepatic
  • fibrosis of bile ducts- sclerosing
  • autoimmune disease
  • obstructive jaundice, bile can leak out into bloodsteram
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19
Q

PBC and PSC

A

Primary bilary cirrhosis autoimmune attack of bile cells in liver, bile can leak into blood and damage liver cells (intrahepatic)

  • can cause cholestasis, obstructive jaundice
  • can get jaundice
  • also can get increase cholesterol
  • can get itchy skin - early itchiness before jaundice
  • get GGT and ALP increase because these are in bile duct cels, and then can also get liver damage due to this
  • AMA antibody positve

Primary sclerosisng cholangitis

  • hardening of tissue of extrahepatic ducts and intra hepatic
  • fibrosis of bile ducts- sclerosing
  • autoimmune disease
  • obstructive jaundice, bile can leak out into bloodstream
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20
Q

*** 3 conditions associated with coeliac disease

A
  • skin conditions - dermatitis
  • 1s degree relative with coeliac disease
  • type 1 diabetes
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21
Q

what are symptoms of cholangitis

A
  • charcots triad
  • fever
  • jaundice
  • RUQ pain
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22
Q

ERCP

A

Endoscopic retrograde cholangiopancreatography

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23
Q

ERCP

A

Endoscopic retrograde cholangiopancreatography

-diagnostic and therapeutic

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24
Q

Side effect of sprinolactone?
candersartan
cilazepril

A

hyperkalemia
not many
dry cough

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25
Q

DEscribe the changes in intra-throacic pressure and volumes that occur during tidal inspiration and expiration

A

The movement of air into or out of his lungs occurs due to pressure gradients. If Patmospheric is greater/more +ve than Palveolar, air will flow into his lungs, and vice versae.
At rest, his atmospheric pressure (Patm) and alveolar pressure (Palv) are 0, and his intrapleural pressure (Ppl) is ~-5cmH20.
During inspiration, his Ppl becomes more -ve, and his alveolar pressure also becomes negative. This pressure gradient betw Palv and Patm causes air to enter his airways.
At the end of inspiration, his Ppl is ~-8cmH20, and his Palv is 0 = equal with the Patm.
During expiration, his Ppl becomes less negative, (e.g. -3cmH2O), and his Palv becomes +ve in order to expel air out into the atmosphere.

His tidal volume is ~500mL

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26
Q

what factors effect systemic atrial baroreceptors

A
  • In chronic hypertension, the entire baroreceptor function curve to shift to the right so that normal firing levels of arterial baroreceptors occur at higher arterial pressures. This is called ‘resetting of the arterial baroreceptors’.
  • Baroreceptor function is also affected by the central nervous system via efferent nerves, which actively set baroreceptor function
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27
Q

short term and long term response of systemic barorceptors

A

Systemic arterial baroreceptors are important in minimising variation in systemic arterial pressure, regulating beat-to-beat arterial pressure, and maintaining blood pressure in the short-term. The extent to which these baroreceptors regulate arterial pressure in the long-term remains controversial. Surgical denervation of arterial baroreceptors led to an increase in the variation of arterial pressure. However the average arterial pressure increased for a very short period before returning to control levels. This indicates that other mechanisms must be involved in maintaining this long-term set point.
Denervation of arterial and cardiac baroreceptors led to sustained hypertension with wide fluctuations in arterial pressure. Thus while systemic arterial baroreceptors do not set the long-term baseline, they do influence the long-term regulation of arterial pressure.

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28
Q

what happens to potassium in diabetic ketoacidosis

A

During the development of DKA, extracellular [K+] increases, due to:
Lack of insulin → decreased Na/KATPase activity → [K+]o increases
Acidosis → impairs Na/KATPase activity → [K+]o increase
High blood osmolarity → fluid from ICF shifts to ECF → ICF [K+] increases → larger gradient between ICF and ECF [K+] → K+ shifts out of cells

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29
Q

Inverted T waves

monomophic ventricular tachycardia

A

i) inverted T waves indicate that repolarisation is occurring in the opposite direction to normal, which can happen in ventricular hypertrophy, bundle branch block, ischaemia.
ii) The electrical activation of the ventricles is not occurring by the usual His-purkinge system, instead electrical activity is travelling from one myocyte to another. This is much slower - hence the wide QRS complexes. This can occur for example if there is a re-entry circuit within a ventricle.

30
Q

clinical features of mitral stensois

A

Diastolic decrescendo murmur heard in the Left 5th intercostal space, mid-clavicular line. Chest X-ray = enlarged LA and pulmonary congestion
Transthoracic ultrasound = narrowed mitral valve orifice, reduced mobility of mitral valve leaflets.
Would expect reduced coronary reserve, and thus reduced exercise capacity (SOB with exertion). May see irregularity of heartbeat.

31
Q

why can we not give a beta blocker and a calcium channel blocker”?

A

Contra-indications =

  • Patients who are on B-blockers shouldn’t go on verapamil too (because both are -ve chronotropes → can lead to heart block)
  • Patients on statins shouldn’t go on verapamil (verapamil inhibits cytochrome P450 C3A4 which breaks down statins)
32
Q

with cyholestiasis why do we get confusion?

A

Increasing liver failure due to cirrhosis can lead to hepatic encephalopathy. This is when ammonia produced by the gut is not able to be metabolised by the liver, and instead is shunted pass the liver to reach the general circulation → passes the blood brain barrier → toxic to the brain → causes CNS issues (concentration affected, sleep cycles…etc)

33
Q

what does lactulose do?

A

Lactulose decreases the pH of the colonic content, thereby preventing ammonia from being absorbed in the gut. It also converts NH3 → NH4 which can then be excreted. Less ammonia in circulation → less enters the brain → symptoms resolve.

34
Q

cholangitis

A

Cholangitis, characterised by charcot’s triad (RUQ pain, jaundice, fever). This is bacterial infection of the biliary tract as a result of obstruction. Obstruction leads to more conjugated bilirubin entering the urine instead of faeces → dark urine

35
Q

why can we sometimes not see blood in stool/

A

Bleeding can be microscopic and so is not always visible to the eye. For example angiodysplasia and some cancers can bleed very small amounts that are not visible to the naked eye. So it does not make bleeding from the colon unlikely.

36
Q

Why there more likely to be a bowel obstruction in the sigmoid colon rather than the caecum?

A

Faecal material in the caecum is relatively loose and has a liquid form. This means that even if there is a large mass in the caecum, it is more likely for the colonic content to pass through the caecum. Whereas in the sigmoid colon, the faecal material is more dense so it can’t pass the sigmoid colon easily. Therefore, patients with sigmoid colon tumour are more likely to present with colonic obstruction.

37
Q

nitroglycerine

A

-increases NO and acts on VSM

38
Q

How can you get arrhythmia during an acute MI?

A
  • ATP reduces
  • Redued Na/K pump
  • increase in sodium inside the cell and potassium outside the cell

Slow conduction - increased extracellular K gives reduces the membrane potenital
-inactivates sodium channels and gives rise to slowed conduction

Reduce AP duration and non-uniform repolarisation - elevated ECF K - reduces AP duration in ischemic region - so get differences in repolarisation rates throuhgout the muscle tissue

After depolarisations

  • reduce ATP - redceud Ca/ATPase - increase in calcium inside teh cell
  • get more ca leave the cell via Na/Ca transporter
  • this gets a large inward current of sodium causing an after depolarisation.
39
Q

what is chest comfort caused by?

A

chemical, mechanical stimuli (eg K+, H+, adenosine) - sympathetic afferents / spinothalamic
- referral to somatic segments of chest & arms

40
Q

What are the symptoms for different QT syndromes?

A

QT1 -
QT2 -
QT3 -

41
Q

What are the symptoms for different QT syndromes?

A

QT1 - stress, exercise
QT2 - auditory stimuli, stress
QT3 - sleep

42
Q

what effect does loratidine have on someone with a long QT syndrome

A
  • anti-histamines - inhibit potassium channels and induce VT in people with LQT syndrome
  • takes longer to repolarise so prolonges QT even more and increases risk
43
Q

How does Long QT work?

A
  • EADs are caused due to a prolonged action potential that enable the calcium L type channels to become reactivated
  • the AP is prolonged in long QT syndrome, and can be further prolonged due to …
  • antihistamines, amiodaone ect.
  • this is because antihistamins block the potassium channels, which leads to a slower entrance of potassium current durign repolarisation
  • there is an increase dispirsion of refractioness so can get renetrant circuit if travel in a unidirectional block aroudn areas of unreporalsied tissue
44
Q

Treatment for Long QT

A
  • beta blockers
  • Implatable cardioveter-defibrillator
  • lifestyle modifications
45
Q

what causes chest discomfort

A

? palpitations

? imparied myocardial perfusion (global ishaemia) ?? pulmonary congestion - poor (LV) pump function.

46
Q

Main changes due to ischeamia causing VT

A

-reduced ATP - reduced Na/K pump - increase extracellular potassium, and increase intraceullar sodium - reduces membrane potential

Slow conduction - increase extracellular K inactivates sodium channels and leads to slowed conduction
-acidosis - decouplign of cell attachments

Reduce AP - hyperkalaemia - redcues AP duration, and reduced ATPase K pump - so get aP duration in ischemic region decreased

Non-uniform repolarisations
-due to some cells undergoign reduced AP and others not

After depolarisations - redcued atp - reduces ATP ca activity, increase in intracellular calcium - get delayed after depolarisations due to increase caclium in cells and SR (increase extrusion of Na/Ca pump) so get more sodium into cell to activate Ap by increase L type channels

47
Q

What to do when have Mi

A
  • ablation of re-entrant circuits after electircal mapign

- can put external defibrillator on

48
Q

what other factors can contribute to electrical instability of the heart?

A

Other factors that can contribute to electrical instability after MI are:
• the increased cardiac sympathetic activity that commonly occurs under these circumstances and
• possible effects of aberrant wall motion on stretch-activated channels.
• aberrant LV wall motion occurs because the mechanical function of the
ischaemic region is impaired.
• for instance, wall thinning and expansion can occur during systole in the infarct region in the presence of wall thickening over the rest of the LV.

49
Q

why likely to get ectopic beats within the first 24 hours

A

Ectopic electrical activation (and reentrant arrhythmias) are most likely to occur in the first 24 hours after MI, because ischaemic myocytes in the region of the infarct and border zone are electrically active, though highly unstable.
• Over the 24 hours post-infarction, the affected cells either die or the ischaemia is resolved.
• NOTE: reperfusion of an infarcted region (as is now common clinically immediately after MI) increases acute electrical instability.

50
Q

GGT alone elevated

GGT and ALP

AST ALT

A
  • statosis - fat in liver cells
  • cholestasis - obstrucive
  • hepatitis, hepatocellular injury
51
Q

What does it mena if have GGT and AST and ALT elevated?

A
  • mixed

- both steatosis and hepatocellular injury

52
Q

If AST >2x ALT -

A

alcoholic hepatitis

53
Q

What are main causes for AST and ALT elevation

A
  • viral
  • ischaemia
  • paracetamol
  • can be if the ast and alt are in the thousands
54
Q

what can low platelet count mean?

A

-signof hypersplenism - protal hypertensio

55
Q

Acute hep B vs chronic

A

-acute - adult transmistion - iv drug use, contaminated blood, sexual - can clear the infection

Chronci hep B - neonate or childhood transmission
-perinatal/vertical and horizontal - undeveolped immune sysetm

  1. Is person currently infectied - yest -surface antigen positiev (HbsAg)
  2. Acute vs chronic - acute - igM present
  3. Cleared infection- surface antigen negative , surface antibodies will be positive and igG postiive

vaccination - only anti-HBs

-need to do blood tests for chronic to see recurrent infections

56
Q

hypoglycaemic

A

-severe liver failure

57
Q

risk factors for people getting HFpEF

A

older, female, hypertensive, diabetic, AF, chronic kidney disease

58
Q

Mechanisms behind diastolic heart failure?

A
  • Relaxation
  • calcium needs to be removed out of cells using ATP, however if have ischaemia cannot get this done as quick - not as much time for relaxation - so not as much time to fill ventricles

Compliance - early phase filling of heart, there is increased stifness of heart wall due to increase modelling - e.g collagen and tinitin so cannot get as much filling.

-overall reduce diastolic volume and also reduced systolic so get ejection fraction normal

59
Q

Mechanisms behind diastolic heart failure?

A
  • Relaxation
  • calcium needs to be removed out of cells using ATP, however if have ischaemia cannot get this done as quick - not as much time for relaxation - so not as much time to fill ventricles

Compliance - early phase filling of heart, there is increased stifness of heart wall due to increase modelling - e.g collagen and tinitin so cannot get as much filling. (passive stretch not as much)

-overall reduce diastolic volume and also reduced systolic so get ejection fraction normal

60
Q

what is pulse presure?

A

going to be large because due to hypertension - are going to have reduced compliance of arteries

61
Q

why shortness of breath worse at night and when lying down

A
  • decrease hydrostatic pressure in legs, get more fluid absorption
  • venous blood distributes around body not stuck in legs any more - increases Right atrial pressure due to increase venous return
  • increase right heart filling - increase pulmonary volume and pressure
  • reduced lung complaince due to increase work of breathing
62
Q

treatments for heart failure

A
  • diet - low salt, diuretics
  • reduce HR - beta blocker (treat if AF present)
  • control Hypertension
  • reduce remodelling - ace inhibitor, ag2 blocker, spirnolactone
63
Q

what are signs on ECG for left bundle branch block>

A

long QRS
william marrow
-activation from right to left side (is delayed)

64
Q

how is this caused?

A

iflammation/firbsois in the myocardium conduciton system in HF

  • leads to discoordinated ocnduction
  • leads to dysyncrhonous contractio and relxation, systolci imparimened and reduce lv fillign time
65
Q

what happens to the mechanical function of the heart by the cardiac electircal function

A

-get bulging of heart msuscle
-get asyncorny because some reagions are contracting and some are not because some are activated and some are nto
-this resutls in poor contraction and relaxation
RV/LV sequence changes
-get slow LV relaxation
-LV systole prolonged
-LV filing time is shortened

-poor blood flow to some regions

66
Q

Who will benefit from cardiac resynchronization therapy ?

A
  • if they still have symptoms even when given therapy
  • QRS > 150
  • LVEF > 30-40%
  • when there isnt a standard thing thats goign worng e.g AV node ..
  • batery operetaed implanted into chest
  • can become a syncronous heart
  • get perfusion better as well
67
Q

what are treatments for AF

A 
AF: Rate control
Ca channel blocker
Beta-blocker digoxin
AF: Rhythm control amiodarone
sotalol - non specific b-blocker (II) & III) dc conversion
ablation therapy ...

Anticoagulant

68
Q

when is there a stridor and when is there a wheeze on expriation

A

Stridor on inspiration due to an increased extrathroacic resistance

  • Expiration is passive, but in this case it is not passive - requires force
  • wheeze on inspiraiton due to narrowed extrathroacic space which causes turbulent flow
  • this is above the level of vocal cord

-if there is a airways colapsing intrathroacic, then get a wheeze on expiration

Stridor is an extrathoracic obstruction, can be due to something like croup. What happens is that normally during inspiration negative pressure is generated in the airways which results in an increased tendency for the airway to collapse, given the extrathoracic pressure placed on the airway this causes airway obstruction during inspiratory phase, increased turbulence and therefore the sound of stridor heard. Expiration is passive and airway pressure is not negative therefore the tendency for the airway to collapse is reduced and no sound is heard on expiration

69
Q

What is another thing that can cause prolonged AP and trigger long QT

A

drugs - amiodarone, sotalol, antihistamine

-reduce extracellular potassium - hypotension

70
Q

why long qt get VT

A
  • get prolonged AP due to potassium and sodium receptor mutations
  • then get L type calcium channels reactivated during this time
  • get an early after depolarisation due to calcium entering - this will be slwo however
  • increase risk of VT - prolonged conduction veloctiy, differnet refractory times, and can get renetrant circuto
71
Q

Treatments for long qt

A
  • if person has already had a cardiac arrest - then give beta blocker and could have an inplantable cardioverter-defibrillatory
  • get beta blocker and lifestyle modificaiton if no previous arrest

RBF (31 decks)

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