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Case 15 Flashcards

1
Q

What is the MABP and how is it calculated ?

A

Mean arterial blood pressure. Degree of vasoconstriction of arterial bed
MABP = CO x TPR (total peripheral R)

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2
Q

How is blood flow calculated and what is the main vessel of resistance?

A

Blood flow = perfusion P / vascular resistance

Aterioles have highest R

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3
Q

What is the difference between the systemic and pulmonary circuits ?

A

Systemic is high P high R

Pulmonary is low , pulmonary artery pressure is 22/10

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4
Q

What is the pressure in the Vena cava ?

A

0-5 mmHg

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5
Q

What are the JVP and Pulmonary wedge pressures estimates of ?

A

JVP , estimate of P variation on R side of heart

Pulmonary wedge = LA

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6
Q

What does the area in a PV loop indicate ?

A

The work done by the heart

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7
Q

What happens in a PV loop after ESV ?

A

End systolic volume. Mitral valve opens blood into LV so V+P ^ as walls resist filling slightly (bottom left to bottom right)

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8
Q

What occurs in a PV loop after EDV ?

A

End diastolic volume. Ventricles filled mitral valve closes. systole begins but all valve shut so no vol change P ^ as isovolumetric contraction begins. (bottom right to top right)

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9
Q

What is happening from top right to top left in a PV loop?

A

Aortic valve opens, ejection occurs rapidly than reduces.

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10
Q

What changes would you see to a PV loop if the ejection fraction was compromised ?

A

Preload ^ so loop moves right and smaller. The contractility may also decrease.

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11
Q

What is the function of arterial baroreceptors ?

A

Found in carotid sinus and aortic arch. Respond to stretch to minimise fluctuations in MABP. Send signals to medulla

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12
Q

Where is the initial processing of baroreceptor info in the medulla and where is the resulting parasympathetic output ?

A

Processing in the NTS (nucleus tractus solitarius)

Para output from nucleus ambiguus

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13
Q

Where are the centres of; defence during stress and thermoregulation ? and circulatory response in exercise?

A

Hypothalamus

Cerebellum

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14
Q

What is the brief baroreceptor reflex ?

A

Bp/B vol down , HR ^ , contractility ^ , peripheral vasoconstriction ^ , ^ BP/Vol

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15
Q

Where are the ‘blood reservoirs’ at rest and what is their function during exercise ?

A

Large veins regulated by SM in walls. CV reserve used in exercise (^ tone)

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16
Q

How does the CV reserve change with age ?

A

With age and/or HF, sympathetic drive decreases as CO/stress on heart already increased due to compensatory mechanisms.

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17
Q

What reflex is antagonists to Baroreceptor reflex and when is it triggered ?

A

Bainbridge. Triggered when B vol is high. Stretch receptors at vena cava.

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18
Q

What is the process triggered by rapid IV saline for example ?

A

Stretches great veins -> ^HR. Shifts blood from congested venous side to arterial side. ^HR by ^RA P due to stimulation of atrial receptors

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19
Q

How does the Bainbridge reflex affect the peripheries and the kidneys ?

A

Doesn’t initiate peripheral vasoconstriction.

Inhibits vasoconstriction in kidneys -> tachycardia +^GFR due to opening to ^ filtration

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20
Q

How is brain blood flow protected by chemoreceptors ?

A

Low ppO2 -> sympathetic vasoconstriction to ^ P and HR

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21
Q

What is the fluid distribution intra/extracellularly and what is the composition of blood within these compartments ?

A

ICF = 15L , ECF = 25L
Blood plasma = 3L ECF
RBC = 2L ICF

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22
Q

What is the dominant cation in the ICF and ECF ?

A

ICF = K , ECF = Na

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23
Q

Why is Na regulation in ECF important ?

A

Makes up 95% of solutes (and osmotic P).
Na drops = vomit, diarrhoea
Na ^ = CHF, cirrhosis, hypertension

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24
Q

What are the fx that influence urine production by nephrons and CD ?

A

glomerular filtration of plasma , tubular reabsorption (proximal absorption of HCO3) and tubular secretion (Distal secretion of H)

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25
Q

What is the formula for GFR?

A

GFR = Kf (ultrafiltration constant) x Puf (ultrafiltration pressure)

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26
Q

What are the 3 fx of ultrafiltration pressure ?

A

Puf = Pgc (glomerular hydrostatic P in afferent arteriole) - Pt (capsular hydrostatic P in the lumen) - πgc (blood cooled osmotic P)

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27
Q

What is the normal value of Puf?

A

10 mmHg

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28
Q

What is the myogenic mechanisms of renal autoregulation of GFR ?

A

systolic BP ^ -> stretch afferent arteriole -> muscle contraction -> diameter done -> BP falls

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29
Q

What is tubuloglomerular feedback ?

A

mediator of vasoconstriction (local adenosine) acts on adenosine-1 receptor on afferent arteriole. ^BP -> ^GFR -> less time for Na/Cl/H2O reabsorption -> JGA detection ^ renin release.

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30
Q

What is the RAAS response to dehydration ?

A

BP down -> JGA ^ renin and angiotensinogen from liver -> AT1 formed goes to lungs -> AT2 via ACE -> vasoconstriction of arterioles and ^ aldosterone so BP ^ and Na/H2O reabsorption ^

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31
Q

What is the effect of the intrarenal PG system ?

A

Locally acting PGs ^ GFR and decrease Na reabsorption by ^LoH and CD flow.

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32
Q

What is HF In lamen terms ?

A

Inability of heart to meet body blood requirements through LV systolic dysfunction. Results in activation of compensatory mechanisms

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33
Q

What are the main causes of HF?

A

Ischaemic heart disease, hypertension, valvular dysfunction, dilated cardiomyopathy

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34
Q

What happens to the sympathetic drive during HF?

A

It increases to ^adrenaline so HR^ and CO^ in compensation

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35
Q

Px goes on HF drugs, what monitoring needs to take place ?

A

Follow up every 2 weeks. close monitoring of pulse, BP and renal function. Refer to nurse led clinics. Telemonitoring

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36
Q

What is LCZ696 ?

A

dual neurohormonal inhibition using Valsartan and Sacubitril to induce hypotension

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37
Q

What is the effect of Sacubitril ?

A

Inhibits Neprilysin (normally breaks down BNP) so natriuretic peptide levels increase

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38
Q

What are the 3 main causes of absolute Fe def in HF ?

A

Malnutrition , malabsorption , GI losses

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39
Q

What inflammatory cytokines ^ during anaemia of chronic disease ?

A

IL-1 , IL-6 , TNF-a

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40
Q

What is the problem with taking aspirin and anticoagulants during IHD ?

A

Ischaemic heart disease

Can lead to GI blood loos -> absolute Fe def

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41
Q

What is OSA ?

A

Obstructive sleep apnoea , collapse of pharyngeal airway. Leads to heavy snoring and disrupted sleep

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42
Q

What feedback is lost during HF that results in sleep apnoeas ?

A

When CO2^/PO2 falls signals normally sent to diaphragm -> contraction -> breathing. This stops in HF

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43
Q

What is apnoea ?

A

Complete cessation of airflow for over 10 seconds

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44
Q

What is the difference between obstructive and central sleep apnoea ?

A 
Obstructive = thoracic/abdo movements still present 
Central = no thoracic/abdo movements, unstable feedback of resp system
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45
Q

What is the AHI ?

A

Apnoea hypoopnoea index; total no events/hour in sleep

5-15 = mild , 16-30 = moderate , 30+ = severe

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46
Q

When is CPAP contraindicated ?

A

For central sleep apnoea -> poorer px outcomes

^ ejection fraction for OSA

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47
Q

When is LA angioplasty pointless ?

A

If >50% tissue scarring in target area because the myocardium won’t be viable and the coronary artery will have no useful function

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48
Q

What is the Batista operation ?

A

Cut open heart, remove scar tissue and mitral valve

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49
Q

How does a ventricular assist device function ?

A

Plugs into apex of heart, sucks blood out and pumps into the aorta. Used in px with poor prognosis. Most require surgery within 1 year.

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50
Q

What are the +ve effects of resynchronisation ?

A

Resynchs LV contraction
^6 min walk past, ^QoL, Cardiopulmonary test VO2 max^
Improves LV ESV and LV EF

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51
Q

What are the major causes of non ischaemic cardiomyopathy ?

A

Ischaemic HD (60%) , cardiomyopathy and hypertension (15%) , valvulopathies (10%)

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52
Q

What is hypertrophic cardiomyopathy ?

A

wall thickness (septum) >15 mm in 1+ segments causes; myocardial fibrosis , abnormalities of MV. Can’t be explained solely by loading conditions

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53
Q

What is ASH ?

A

asymmetrical septal hypertrophy. Stiffness requires ^ P to fill up. P comes from atria -> atrial dilation. Tract for blood v small -> velocity of blood ^ , P grad pulls mitral valve toward septum so hole becomes even smaller

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54
Q

How does HCM commonly present ?

A

Syncope, arrhythmia, baroreflexes, LVOT obstruction. Possible dyspnoea, diastolic dysfunction , AF (stroke) , MR.

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55
Q

How would HCM show on an ECG ?

A

Sinus rhythm, atrial fibrillation, ST segments , T wave inversion

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56
Q

What is the medical therapy for LVOT obstruction?

A

(Non dilating b blockers or Verapamil) with disopyramide (a Na channel blocker)
If using b blockers monitor QT

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57
Q

What is alcohol septal ablation ?

A

Catheter in LAD, inject dye and balloon into septal branch. Then insert alcohol to destroy muscle/tissue and initiate infarct to decrease septal buldge.

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58
Q

What is DCM ?

A

Dilated cardiomyopathy, cardiac enlargement with decreased systolic function. No primary valve disease or significant CAD.

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59
Q

What is an Epsilon wave and along with T wave inversion of V1-V3 what would it indicate ?

A

Small positive deflection buried in QRS. May look like an M at the end of QRS.
Arrhythmiogenic RV cardiomyopathy

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60
Q

What is ARVC ?

A

fibro fatty infiltration, ventricular dilation and hypertrabeculation

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61
Q

What is RCM ?

A

restrictive cardiomyopathy. Normal cardiac size with decreased systolic/diastolic function and bilateral dilation. Usually from an MI

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62
Q

How does presentation of RCM change between males and females ?

A

Later in females because protein build up is slowed due to periods. Present post menopause

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63
Q

What is amyloid disease ? What does an ECG show ?

A

Cardiac deposition of abnormal protein load. Hypertrophy but normal complexes on ECG.

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64
Q

What is the cardiothoracic ratio? What is the normal for adults ?

A

On a CXR, the ratio of distance between horizontal borders of the heart and the distance between the ends of the rib cage. Normal is 0.5 in adults. May be slightly ^ in kids and athletes.

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65
Q

What is a systolic murmur ?

A

Heart in ejecting phase. Abnormal sound from closure of tubes or turbulent blood flow eg. aortic valve stenosis or mitral regurgitation.

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66
Q

What is an S4 systolic murmur and what are the risk fx?

A

Sound proceeding S1 late diastole just before valves (LV) shut due to stiffness/lubrication.
Age, chronic hypertension, genetics.

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67
Q

When is an S3 diastolic murmur heard ?

A

Early diastolic from rapid chamber filling.

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68
Q

What are the sounds for S3 and S4 respectively ?

A 
S3 = sloshing-ing IN
S4 = AT stiff wall
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69
Q

What are crepitations ?

A

Crackling sound breathing in as the airways ‘pop open’

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70
Q

What is a bruit ?

A

Abnormal sound in an artery. Possible renal artery stenosis, aortic dissection.

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71
Q

What is delirium ?

A

Acute cognitive impairment due to another medical condition. Can improve for up to 6 months after.

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72
Q

What is sarcopenia ?

A

Clinically; Loss of muscle strength

Ageing (1st) and HF (2nd) causes. Deconditioning worsens sx.

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73
Q

What is frailty ?

A

Accumulation of deficits in multiple organ system over time. More prone to negative outcomes due to decreasing homeostatic reserve.

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74
Q

What is the difference in BP between men and women ?

A

20-25 healthy male 75 Kg normal BP = 120/80

A women would be around 10 below this.

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75
Q

What is essential hypertension?

A

Idiopathic (95% of cases). Possible causes; fewer nephrons, impaired renal Na excretion so ANP^, overactivity of RAAS.

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76
Q

How does LVH arise from chronic hypertension ?

A

Left ventricular hypertrophy. Sacromeres added in parallel to original ones, thickens wall -> CHF with dilatation of the heart. Hypertrophy compromises SV initially then fails -> congestion.

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77
Q

Where does vascular wall thickening occur and why?

A

Result of ^BP, media of muscular arteries (hyperplasia of muscle and collagen deposition -> stiffness). Overall decreases compliance.

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78
Q

What is hyalinisation ?

A

cause of renal failure possibly from chronic HT. Proliferation of small BVs and deposition of large proteins, in this case Fibrinogen in media layer of glomerulus and arterial walls.

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79
Q

How do GFR and RAAS effect BP ?

A

GFR down -> ECF^ -> ^CO (higher preload) -> ^BP

RAAS ^ -> Na reabsorption and ECF increase which follows on to ^BP.

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80
Q

CO is increased through fluid expansion of ECF. How does this happen ?

A

GFR down, ^Na reabsorption, RAAS^ , Sympathetic drive ^ (nerves stimulate JGA to secrete renin)

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81
Q

What fx affect Na reabsorption in the PCT and DCT ?

A 
PCT = AT2 
DCT = aldosterone effect
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82
Q

What substances cause a decrease in CO ?

A

renal PGs (auto reg of the kidney) and PGE2 inhibit salt and water retention. This reduces ECF volume, decreasing CO.

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83
Q

What is the effect of peptides relative to essential hypertension ?

A

Peptides inhibit pumps in SM arteriole walls. ^intracellular Na so decreases pumps. This ^Ca causing vasoconstriction and TPR increases.

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84
Q

What are the iatrogenic fx for hypertension ?

A

Taking; COCP, NSAIDs (^intrarenal PGs so effect kidney filtration) , steroids, chronic vasoconstriction meds

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85
Q

What is Liddle’s syndrome?

A

^BP in early life due to ^ expression of epithelial Na channel in CD. ^reabsorption of Na. v rare.

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86
Q

What is metabolic syndrome ?

A

HT associated with obesity and insulin resistance. ^PCT Na/H exchange.

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87
Q

Where is the most resistance in circulation ?

A

Peripheral ends of the arteriole tree. Site of most damage. Eye tests give good indication of vasculature

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88
Q

How do blood volume pathologies arise ? What happens to the internal disc lamina ?

A

Repetitive stress from HT changes to medial layer esp SM hypertrophy (tunica media) ^TPR and BP.
Internal disc lamina becomes reduplicated and interrupted. Hyaline degeneration -> glassy eosinophilic material ^ -> rigidity.

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89
Q

How would fibroid necrosis in an artery look histologically?

A

Wall is bright pink with dark neutrophils.

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90
Q

What is nephrosclerosis ?

A

Shrinking of glomerular BM (poor perfusion) , hypertrophic and hyaline depositions in afferent arterioles -> sclerosis. Tubes become ischaemic -> atrophy and fibrosis (nephrosclerosis).

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91
Q

Name a diuretic and give a + and - outcome of use ?

A

Chlorothiazide. Coexistant CCF adjunctive with other agents.
May cause electrolyte/metabolic ADRs and allergies.

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92
Q

What is the first stage of mx in HT?

A

Confirm persistant HT on multiple occasions. Modify reversible lifestyle fx. Investigate end organ damage (esp heart, kidney). Look at other vascular risk fx eg. plasma lipid profile. Screen for 2ndry HT causes.

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93
Q

What is renal parenchymal disease ?

A

Loss of vasodilation then retention of Na/H2O leading to ECF ^. Cause of secondary hypertension.

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94
Q

What is Conn’s syndrome ?

A

adrenal cortex tumour secretes aldosterone no matter regulation. -ve feedback on Renin (decreases) so aldosterone:renin ratio ^. Possible metabolic alkalosis.

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95
Q

What condition would show a normal aldosterone:renin ratio even though aldosterone has ^ ?

A

Coronary HF, ^aldosterone but no compensation so BP stays ^. RAAS stays active so ratio normal

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96
Q

What is adrenal medulla pheochromocytoma and how would you test for it ?

A

Adrenal tumour secreting catecholamines. BP spasms up and down quickly. 24 urine test recording catecholamine levels.

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97
Q

What is the difference between the renal parenchyma and the collecting system ?

A

Parenchyma, functioning kidney that filters blood and makes urine
Collecting system, urine produced by parenchyma then filtered moves urine out of kidney into ureter then into bladder

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98
Q

What is the outline of the Goldblatt experiment ?

A

clipped kidney hypoperfused (thinks BP down) so ^ renin -> vasoconstriction/BP^. Perfusion restored at higher BP.
Healthy kidney drops renin but no natriuretic response so Na not compensated (mystery). Intrarenal AT2 stays high in healthy kidney.

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99
Q

What are the 3 fundamental features of HF ?

A

Haemodynamic changes (^plasma vol to try ^CO) , Metabolic effects (decrease coronary flow, ^stress to myocardium) , neurohormonal changes

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100
Q

How is SV maintained through ‘compensation’ ?

A

Filling pressure increases. Vol ^ early in HF to ^preload and decrease CO.

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101
Q

How does the EDV change over time during compensation?

A

Over time hearts contractility decreases so EDV at rest ^ to compensate. Smaller window of compensation with exercise.

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102
Q

What is the cause of diastolic HF ?

A

delayed relaxation and impaired filling. Typically seen in px with cardiac hypertrophy.

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103
Q

Name 3 metabolic events that occur through HF ?

A

Impaired blood flow (ischaemia, Ca pumps breakdown cells begin to swell as osmolarity ^ -> cell death)
Inflammation, vol overload venous congestion -> neutrophil, compliment activation -> cell death
Anaemia, renal dysfunction causes poor formation of EPO.

104
Q

How does AT2 exert negative feedback ?

A

acts on AT1 receptor in JGA to decrease renin secretion.

105
Q

What happens when AT2 negative feedback fails ?

A

If ^ blood volume doesn’t decrease BP then renin production not inhibited. Instead vol ^ , Cardiac function decreases and decomposition occurs.

106
Q

When can the adaptive ^ of AT2 in circulation be counterproductive ?

A

Scarring occurs as direct result of HF because BP first decreases from AT2 but then ^ as AT2 triggers other stressors.

107
Q

What are the common signs of HF ?

A

JVP elevation, wheeze, tachypnoea, sweaty, S3 gallop rhythm, ascites/hepatomegaly, cyanosis/pallor, palpitations/tachy/brady, rapid weak pulse, peripheral oedema

108
Q

List some possible clinical features of HF ?

A

Reduced O2 sats (<90% pulse oximetry) , hypoxaemia , acidosis, elevated blood lactate >2mmol , oliguria (urine output <0.5 mL/Kg/h)

109
Q

What would be the first line diagnostic tests for HF ?

A

Echocardiogram and then BNP

110
Q

What is BNP ?

A

Peptide secreted by the ventricles of the heart in response to excessive stretching of myocytes.

111
Q

Why is BNP a better marker for HF than ANP ?

A

Longer half life, less potent.

112
Q

What are the causes of peripheral oedema ?

A

Neurohormonal activation (aldosterone causes Na reabsorption, ADH causes H2O reabsorption) , ^CVP (^RA P) , Low albumin (Oncotic P down fluid out of capillaries) , Venous disease (DVT -> leaky valves) , immobility (blood pools in extremities) , ^Pelvic P (no blood returning if IVC compressed)

113
Q

When might the IVC be compressed leading to peripheral oedema ?

A

Pregnancy and uterine tumours

114
Q

What are the 3 key roles of Ca ions ?

A

Vascular SM contraction via IP3 signalling (^afterload) , cardiomyocyte cell contraction via ryanodine , Cardiac electrical conduction (AVN slows impulses)

115
Q

How would a L HF show on an echocardiogram ?

A

dilated ventricle, wall thinner and shows weaker contraction -> backlog of fluid in chamber. ^Vol due to ^blood V after ejection

116
Q

What is pitting oedema ?

A

Peripheral oedema where the indent remains after point pressure released.

117
Q

How do the cardiomyocytes change during ventricular hypertrophy ?

A

Larger and ^no but less efficient. They try and compensate for ^afterload so chamber V and CO decrease.

118
Q

What is the difference in terms of ejection fraction between systolic and diastolic HF?

A

Systolic; weak contraction with decreased ejection fraction

Diastolic; compromised relaxation but preserved ejection fraction.

119
Q

Why is ejection fraction preserved during diastolic HF?

A

Stiffened ventricle walls so difficult to fill in diastole

120
Q

What is the significance of ARB selectivity ? Give an example…

A

Selective for AT1 receptors so more AT2 binds to AT2 receptors causing vasodilation. CandeSARTAN

121
Q

What is the mechanism that a b blocker inhibits through occupation of the b1 adrenoreceptor ?

A

adrenoreceptor ^ activation of cations -> ^automaticity in the nodes or Ca in the myocytes -> HR/inotropy.

122
Q

When would you give Digoxin?

A

If dry on acute admission to ^fluid, need a +ve inotrope.

123
Q

What is the overall function of diuretics ?

A

Trap ions in the urine preventing osmosis of H2O from urine into blood. Therefore diuresis occurs through ^ urine volume.

124
Q

Name a loop acting diuretic, what is its function and when is it indicated ?

A

Furosemide inhibits Na/Cl/K symporter (mainly Cl) in ^limb cells. Dilutes urine by retaining ions.
HF with associated oedema, can cause hypokalaemia

125
Q

What is Bendroflumethiazide ?

A

Thiazide like diuretic that inhibits Na/Cl supporter in early DCT. Traps Na (and therefore H2O) in urine

126
Q

Name a common K sparing diuretic, why is it considered weak ?

A

Spironolactone , low amount of Na normally absorbed in the principal cells of the CD.

127
Q

What is the MOA of Spironolactone ?

A

Antagonises aldosterone receptor that allows Na into blood through Na/K ATPase

128
Q

How is K normally regulated in the kidney ?

A

NaK ATPase (driven by Na current) moves Na into blood and K into cell. ROMK (renal outer medullary K pump) then puts K in the urine.

129
Q

What is the downside to loop and thiazide like diuretics ?

A

Can cause hypokalaemia because they ^K excretion. When tx check renal function, U+Es and K levels on admission.

130
Q

What are three major functions of the kidneys ?

A

Produced erythropoietin (regulates RBC production) . produce Renin (regulates Na via aldosterone secretion) , synthesises 1,25-dihydroxycholecalciferol from Vit D (stimulates Ca absorption from the gut and calcification of bone)

131
Q

What is the anatomical position of the kidneys ?

A

Either side of vertebral column at T11-L3

132
Q

What is the hilus of the kidney?

A

Indentation in the midline, entrance for renal artery and exit for renal vein and ureter.

133
Q

Which part of the kidney contains the renal BVs and is the origin of the ureter ?

A

Renal pelvis. Outer cortex and inner medulla and renal pelvis

134
Q

What is the central space of the kidney called and what is its function ?

A

Major calyx , divided into minor calyces that collect urine from renal papillae

135
Q

What is the make up of the epithelial cells of the PCT ?

A

Cubodial, rich in mitochondria, connected via tight junctions near apical surface. Covered by microvilli (brush border)

136
Q

What is the difference between the descending and ^ limbs of LoH in terms of mitochondrial density ?

A

^ is very dense (more active transport of ions). Down is less dense.

137
Q

What types of cells are in the epithelium of the collecting ducts ?

A

Principal ‘P’ cells - regulate Na balance

Intercalated ‘I’ cells - regulate acid base balance

138
Q

What supplies the renal cortex up to the afferent arterioles ?

A

Sympathetic paravertebral chain (T12-L2) supply renal cortex up to afferent arterioles. Adrenergic supply.

139
Q

What supplies the efferent arterioles of the kidneys ?

A

Vagal parasympathetic fibres innervate the efferent arterioles. Cholinergic supply.

140
Q

What is the significance of the vagal innervation to the kidney ?

A

Provides extrinsic control for renal circulation that can override the intrinsic autoreg of blood flow.

141
Q

What is the myogenic hypothesis of renal auto regulation ?

A

Renal arteries stretch ^P -> distends arteriole wall and stretches SM fibres -> contraction -> ^R and reduces blood flow.

142
Q

What is the metabolic hypothesis of renal auto regulation ?

A

Metabolites from renal tissue maintain vasodilation ^perfusion P -> ^blood flow -> ^metabolites so decrease the vasodilation.

143
Q

What are the effects of A/NA , AT2 and ADH generally ?

A

Circulating A/NA -> vasoconstriction in renal circulation (NA acts on renal cortex)
AT2/ADH act as powerful vasoconstrictors

144
Q

How does vasoconstriction in the afferent and efferent arterioles affect P ?

A

In the afferent -> reduces P in glomerular capillaries

In the efferent -> ^P

145
Q

What are the 3 components of the barrier wall that restrict the passage of fluid into the Bowman’s capsule ?

A

Capillary wall (endo wall small gaps ‘fenestrae’ , only permeable to H2O) , BM (fibrils of -ve charged glycoproteins) , Podocytes (extend pedicels - thin processes allowing slits for filtration)

146
Q

The barrier is more permeable to specifically charge ions , which charge ?

A

Neutral or +ve charged ions.

147
Q

What is the renal clearance ?

A

Vol of plasma cleared of a given substance in 1 min. substance

148
Q

What is the renal threshold for glucose ?

A

Value (10-12 mmol/L) at which glucose appears in urine. Slow ^ then rapid >17 mmol/L as transport processes become fully saturated.

149
Q

What happens if the GFR is unbalanced relative to the transport capacity of the tubules ?

A

Too small and the kidneys will be unable to regulate internal environment.
Too large results in loss of vital nutrients from the body.

150
Q

What happens to GFR and the arterioles when systemic arterial BP ^ ?

A

Renal blood flow and GFR remain stable. ^diameter of afferent arterioles -> arteriolar constriction to return to normal.

151
Q

How does auto regulation apply to haemorrhage ?

A

ADH^ -> vasoconstriction. decreased urine (anuria) but normal plasma V (^H2O reabsorption/vasoconstriction) so offsets fall in BP.

152
Q

What are the Na/glucose transporters in the PCT and basolateral membrane tubules ?

A

PCT; proximal = SGLT2 (low affinity) , SGLT1 (high affinity

Basolateral membrane = Proximal GLUT2 (low affinity) and distal GLUT1 (high affinity)

153
Q

What is the difference between trans and paracellular transport ?

A

Transcellular; via tubular cells through secondary AT

Paracellular; between cells via diffusion

154
Q

How does excess PO4 lead to the demineralisation of bone ?

A

PO4 binds to Ca, decreasing production of calcitriol. Decreases Ca uptake by the gut, this ^parathyroid secretion and causes demineralisation.

155
Q

Where is PO4 absorbed? What is the carrier? What proportion is excreted in the urine?

A

SLC34 carriers absorb PO4 in brush border PCT. Some in DCT so 15% excreted into urine. No absorption by LoH/CD

156
Q

What hormone regulates PO4 reabsorption and how ?

A

PTH binds to receptors of PCT -> GPCR activate Gs -> cAMP -> pKa -> removes transporters to be degraded by lysosomes. So ^PTH = ^PO4 excretion

157
Q

7g of protein reaches the PCT each day, how is it reabsorbed ?

A

thin cells engulf it through ‘pinocytosis’. Proteins bind to ‘megalin’ and ‘cubulin’ receptors. They form vesicles which fuse with lysosomes.

158
Q

What can proteinuria indicate and what does it look like ?

A

Frothy urine as protein lowers the surface tension.

UTI, damage to glomerulus, HT, preeclampsia.

159
Q

Where is Ca absorbed and through which channel ? What hormone can ^ uptake ?

A

DCT, TRPV5 and 6 (Transient receptor potential cation channel).
PTH activates PHT receptor -> ^expression of Ca transport proteins in DCT

160
Q

What produces ADH and how is it regulated ?

A

Produced by supraoptic and paraventricular nuclei then stored in PPG. Secretion regulated by osmoreceptors in hypothalamus.

161
Q

During bladder suppression in spinal shock, when is micturition trigged ?

A

Loss of descending control so reflex lost. Instead when threshold reached ‘automatic bladder’ leads to periodic voiding of urine.

162
Q

How is micturition normally inhibited and facilitated ?

A

Inhibited by hypogastric (sympathetic) and pudendal nerves

Facilitated by pelvic (para) nerves

163
Q

What is chronic renal failure and what are the signs ?

A

Long period of >3/4 functional tissue lost. GFR falls below 25 (normal 120).
Urea conc in blood ^ , acidosis -> CNS depression, coma, death

164
Q

How does glomerulonephritis lead to hypertension ?

A

inflam-> occlusion. PCT absorbs more Na so less reaches macula dense so renin^ -> aldosterone -> more Na reabsorbed at DCT -> fluid retention -> HT

165
Q

What are the 3 main causes of HF?

A

Ischaemic HD, hypertension, cardiomyopathy

166
Q

What is outflow resistance and what factors influence it ?

A

afterload. Load/R against ventricular contraction.

Pulmonary systemic R, vessel wall characteristics, blood V ejected.

167
Q

What happens as after load ^ ?

A

As afterload^ CO decreases which leads to ^end diastolic volume

168
Q

What is Laplace’s law ?

A

Tension of myocardium proportional to intraventricular P multiplied by the radius of ventricular chamber

169
Q

How does sympathetic activation help rectify CO acutely and does this become a problem chronically during HF?

A

Sympa activated via baroreceptors ^inotropy maintains CO.

Chronic activation -> neurohormonal activation and myocyte apoptosis

170
Q

What is cardiomyopathy ?

A

Progressive ventricular dilatation/hypertrophy without ischaemic myocardial injury or infarction

171
Q

How does the myocardial gene expression change during myocardial remodelling in HF?

A

P overload results in shift from a to b myosin heavy chains in the atria (already b in ventricles). Lower atrial contractility but lower energy demands

172
Q

What is ANP, where is it released from, what are its triggers, what are it’s functions, what happens to levels during CCF ?

A

Atrial natriuretic peptide
Released from atrial myocytes in response to stretch
Induces; diuresis, natriuresis, vasodilation, suppression of RAAS
Levels ^ during CCF

173
Q

What is C type peptide ?

A

Similar action to ANP but limited to the vascular endothelium and CNS

174
Q

What stimulates endothelin release ?

A

Hypoxia, catecholamines, AT2

Main source is pulmonary vascular bed.

175
Q

What are the actions of endothelin that may contribute to HF?

A

Vasoconstriction, sympa stimulation, RAAS activation, LV hypertrophy

176
Q

What are the common sx of HF clinically ?

A

exertion dyspnoea, orthopnea, paroxysmal nocturnal dyspnoea, fatigue

177
Q

What are the common signs of HF clinically ?

A

^JVP, cardiomegaly, 3/4th heart sounds, bibasal crackles, pleural effusion, peripheral oedema, ascites, hepatomegaly

178
Q

What is the NYHA classification of HF?

A
  1. no limitation
  2. normal physical activity -> sx
  3. gentle physical activity -> sx
  4. Rest -> sx (worsened by activity)
179
Q

What are the 3 conditions needed to diagnose HF-REF?

A

HF with reduced ejection fraction

Sx and signs typical of HF, reduced LV ejection fraction

180
Q

What features of a CXR indicate HF?

A

Cardiomegaly, pulmonary congestion with upper lobe distension, fluid in fissures, Kerley B lines, pulmonary oedema

181
Q

What is the purpose of cardiac catheterisation ?

A

Dx of IHF, measure pulmonary artery P, LA wedge P, LV end diastolic P

182
Q

What is the overall function of diuretics ?

A

^Renal excretion of salt/H2O by blocking tubular reabsorption of NaCl. Given to px with fluid overload. ^sx of dyspnoea and ^ exercise tolerance.

183
Q

What are the ADRs of ACEis?

A

Cough (dry) , hypotension, hyperkalaemia, renal dysfunction

184
Q

What is Nebivolol ?

A

b blocker used in px >70 with HF if stable mild/moderate.

185
Q

What is the action of Ivabradine ?

A

Decreases HR without affecting BP. Inhibits If channels (funny current) in SAN.

186
Q

What tx would you explore if px had stage B HF?

A

Structural heart disease with no sx

ACEi/ARBs in all with b-blockers in some

187
Q

Px has refractory sx of HF and requires special intervention. What tx would you give them?

A

Inotropes , VAD, transplantation etc

188
Q

What is CRT ?

A

Cardiac resynchronisation therapy. Pacing of both ventricles using leads in RV and coronary sinus to pace LV. Works in LV impairment and ^QRS (LBBB)

189
Q

What are the causes of pulmonary oedema ?

A

Ischaemic HD, valvular HD (regurgitation) , HT , kidney disease (fluid overload and reduced renal excretion) , atrial fibrillation

190
Q

What levels of BNP and NT-proBNP suggest HF ?

A

BNP >100 pg/ml

NT-proBNP >300 pg/ml

191
Q

What are the effects of ^compliance of the aorta ?

A

steadier flow to the tissues, fluctuations of flow decrease, small oscillations of arterial P

192
Q

How is SM relaxation inhibiting directly and indirectly via pharmacological tx ?

A

Directly inhibit Ca entry through Nifedipine

Hyperpolarise the membrane indirectly decreasing Ca through K activators eg. Minoxidil.

193
Q

What is the effect of PGE2 on sympathetic nerve terminals?

A

Direct vasodilator inhibits NA release from sympathetic nerve terminals

194
Q

Which vasoactive peptides are secreted by the endothelium ?

A

C-natriuretic peptide, acts on cGMP
Andrenomedullin (vasodilator) acts on cAMP
AT2+endothelin, potent vasoconstrictors

195
Q

When can VEGF’s repair process and pathogenesis cause negative effects ?

A

Neovascularisation in the eye, cause of blindness in px with DM.

196
Q

What substances stimulate and inhibit endothelin release ?

A

Stimulate; A, AT2, ADH, insulin, cortisol, IL-1

Inhibited; shear stress, PGI, NO, natriuretic peptides.

197
Q

What are the functions of endothelin ?

A

^release of ANP, aldosterone, A, HPA axis activation
Natriuresis and diuresis
Renal and cerebral vasospasm

198
Q

What stimulates renin secretion ?

A

Reduced renal perfusion P, reduced Na conc in DCT (sensed by macula densa) , renal sympa nerve activity, b-adrenoreceptor agonists

199
Q

What are the actions of AT 3 and 4 ?

A 
3 = ^aldosterone and thirst 
4 = ^plasminogen activator inhibitor-1
200
Q

What is the effect of ADH when bound to V1 and V2 receptors ?

A 
V1 = vasoconstriction at ^conc ADH through activation of phospholipase C 
V2 = H2O retention at low conc of ADH through activation of adenylyl cyclase in renal CD.
201
Q

What is Minoxidil ? What is a common side effect ?

A

Long acting vasodilator targets K channels. Used as last resort in severe HT. Causes hirsutism (male pattern hair growth in women)

202
Q

What is Levosimendan ?

A

Activates K channels and ^ sensitisation of cardiac contractile mechanism to Ca by binding troponin C. Used in decompensated heart failure

203
Q

What is the action of dopamine ?

A

Selectively dilates renal vessels ^cAMP by activating adenylyl cyclase. When given IV acts on a/b adrenoceptors BP^ but mainly vasodilation in renal circulation and ^CO

204
Q

What are the overall effects of vasodilator drugs ?

A

^local tissue blood flow, reduce arterial P, reduce central venous P. Reduce C preload (reduce filling P) and after load (reduced vascular R) hence reduction of cardiac work

205
Q

What is Aliskiren ?

A

Renin inhibitor used in essential hypertension.

ADRs; diarrhoea (common) , hypotension, renal impairment

206
Q

Why do ACEi cause a dry cough ?

A

Accumulation of bradykinin, may also cause angioedema (pain swelling in tissues, life threatening if involves airway).

207
Q

What is Doxazosin ?

A

Long acting a1-adrenoreceptor antagonist , improves sx of prostatic hyperplasia (benign prostatic hypertrophy). Can cause postural hypotension

208
Q

What is the difference between Conivaptan and Tolvaptan?

A

Conivaptan, non selective antagonist to V1/2 receptors

Tolvaptan, selective V2 receptor used for hypervolaemia and hyponatraemia

209
Q

What is shock ?

A

Inadequate perfusion of vital organs, usually due to low arterial BP. Anaerobic metabolism -> ^lactate

210
Q

What is peripheral vascular disease ?

A

Atheroma in peripheral arteries, first sx is pain in calves on walking. Can progress to other vascular beds (coronary, cerebral, renal)

211
Q

What drugs would be used to treat peripheral vascular disease ?

A

Antiplatelet drugs (aspirin, clopidogrel) , a statin (simvastatin) , ACEi (ramipril)

212
Q

Px presents with sx of CHF, angina and exertional syncope. On exam there’s thrusting apex beat and a systolic ejection murmur at the upper R sternal border. What’s the dx ?

A

Aortic stenosis

213
Q

What are the indications of mitral regurgitation ?

A

Acute; pulmonary oedema

Chronic; exertion dyspnoea and lethargy. A pansystolic murmur is audible at the apex.

214
Q

What conditiosn produce systolic murmurs ?

A

Mitral regurgitation and aortic stenosis.

215
Q

Px presents with SOB, bi-basal crepitations and ankle oedema. Hx of MI, what tests should you do ?

A

Echocardiogram

BNP/NT-proBNP test

216
Q

Px receiving tx for chemo for her HER2 +ve breast cancer. Why does she require regular cardiac screening ?

A

May be at ^ risk of dilated cardiomyopathy

217
Q

What phase of SAN AP does bisoprolol affect in its mechanism of action ?

A

Phase 4

218
Q

Why is the aorta predisposed to an aneurysm more than any other vessel in the body ?

A

Aorta is the artery with the greatest wall tension

219
Q

Why are AAAs more common than thoracic ?

A

Lower elastin content in abdominal

220
Q

What are the ways of measuring degree of heart failure ?

A

Ejection fraction of the heart

Longitudinal axis LV function

221
Q

What is the order of waves for a JVP waveform ?

A

a, c, x, v, y

222
Q

What does each JVP waveform correspond to?

A

A; late diastole, atria contract tricuspid open
C; begin systole, atrial kick. Tricuspid fully closes in ventricular systole
X; Atria relax and fill.
V; P^ in atrium, Tricuspid opens blood into ventricles. End of systole
Y; atria empty tricuspid fully open. Begin diastole

223
Q

Why would you get a large A wave on JVP waveform ?

A

Complete heart block (uncoordinated atria and ventricles so atrial P^) , pulmonary HT

224
Q

What would you see on a JVP waveform if px had tricuspid regurgitation ?

A

Large V wave, ^RA pressure so blood back through valve

225
Q

Why would a steep Y descent be seen on JVP waveform ?

A

Constrictive pericarditis. RA P lower than before so RV can’t fill

226
Q

What is the mechanism of Candesartan?

A

Highly selective AT1R, can shift balance of receptors AT2 bind to, binding to AT2R instead

227
Q

What condition may show an absent a wave on JVP ?

A

Atrial fibriliation

228
Q

Which part of the nephron does Furosemide act on ?

A

Na/Cl/K channel of thick ascending limb

229
Q

What genetic condition can ^the risk of DCM is a gene carrier ?

A

Duchennes muscular dystrophy

230
Q

CXR shows horizontal lines at the base of the lung, what does this mean ?

A

Interstitial pulmonary oedema

231
Q

65 female with chest pain. ECG shows broad QRS at 135 bpm with single foci in ventricles. What is most likely dx ?

A

Monomorphic ventricular tachycardia

232
Q

What ion channel to thiazides have greatest therapeutic action on ?

A

Na/Cl transporter in the DCT

233
Q

What effect might bipolar tx have on ADH ?

A

Lithium is a tx for bipolar. Causes collecting duct to stop responding to ADH -> low osmolarity of the urine

234
Q

What is arrhythmogenic right ventricular cardiomyopathy? What are the signs on an ECG?

A

Cause of sudden cardiac death, fatty infiltrations, dilation of RV (and/or LV), T wave inversion in V1 and V3

235
Q

What is a cheat way of indicating axis deviation on an ECG ?

A

QRS complexes in leads 1 and 3 point away from lead 2 (leaving) then it’s left deviation
QRS complexes point inwards then its (returning) right deviation.
Normally they all point upward

236
Q

What are the causes of the 3rd and 4th heart sounds ?

A

3rd; tensing of corda tendenae and atria, suggests ventricular dilation
4th; poor ventricular function, either aortic stenosis of HT. Common in the elderly

237
Q

What does the INR measure ? What is added to the sample

A

Extrinsic pathway activity. Ca added to replace removed levels and plasma added to substitute for tissue fx.

238
Q

Which fx has the shortest half life so decreases most rapidly in the INR test ?

A

Factor 7

239
Q

What do high and low INR result indicate ?

A 
High = prone to bleed 
Low = prone to thrombosis
240
Q

What is the APTT?

A

Activated partial thromboplastin time, assesses intrinsic pathway.

241
Q

A women has HF from aortic stenosis. What order would signs present ?

A

^intraventricular P as ventricle try to pump blood across valve. This causes back log of blood into lungs (pulmonary oedema) therefore Crepitations seen. Fluid continues to build until effusion -> R sided HF -> JVP^ and peripheral oedema.

242
Q

What is the acute tx of a STEMI ?

A

Morphine, O2, anti platelet (aspirin 300mg)

243
Q

What is the most common cause of HF ?

A

Ischaemic HD > primary cardiomyopathies > HT

244
Q

What does basal crepitation indicate ? what could be a cause ?

A

Pulmonary oedema, often due to chronic pulmonary HT secondary to LVHF

245
Q

What are the causes of ankle oedema ?

A

R sided HF from cor pulmonale, tricuspid valve pathologies or cardiomyopathies

246
Q

What is the course of action if chronic HF is suspected ?

A

ECG -> BNP -> Echo

247
Q

What drugs are 1st line for acute decompensation of chronic HF ?

A

Furesomide and Ramipril (+/- beta blocker)

248
Q

What could a systolic murmur indicate ?

A

Mitral regurgitation (pan systolic) or aortic stenosis (ejection systolic)

249
Q

Where would the murmur radiate for AS and MR ?

A

Aortic stenosis - carotid artery

Mitral regurgitation - left axillary region

250
Q

When are S3 and S4 heard ?

A

S3, early diastole in passive filling (elastic limit reached)
S4, last diastole during strong atrial contraction/filling

251
Q

How do you calculate dilution factor for a drug ?

A

Actual concentration of given drug divided by required concentration for particular px

252
Q

Which diuretic drug has an ADR of gynaecomastia ?

A

K sparring diuretic - Spironolactone

253
Q

How do you differentiate absolute iron def from erythropoietin def ?

A

GFR would be <30 and cytokines ^ with erythropoietin.

Absolute Fe causes GI blood loss or from malnutrition.

254
Q

How would you differentiate between HCM and RCM on echo/ECG ?

A

HCM - LVOT obstruction with reduced chamber size

RCM - small QRS on ECG. walls might be thicker but chamber size is normal

255
Q

What values of ejection fraction correspond to concern ?

A

50% is reduce , 40% is ‘systolic HF’ and under 30% is severe

256
Q

What is the most common cause of 2ndry HT and list 4 others ?

A

Renal parenchymal disease

1/2ndry hyperaldosteronism , renal ischaemia, pheochromocytoma

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