1 Flashcards

(96 cards)

0
Q

Describe the baroreceptors reflex with high blood pressure

A

Baroreceptors are activated by stretch, increased firing rate causes increased parasympathetic output via vagus nerve to lower heart rate and blood pressure

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1
Q

Where are baroreceptors located?

A

Aortic arch and carotid sinus

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2
Q

Describe the baroreceptors reflex with low blood pressure

A

Decreased firing rate causes increased sympathetic outflow (and inactivated vagal neurones) causing increased CO and SV to raise BP

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3
Q

Where is ANP released from and what is its purpose?

A

Released from Atrial myocytes in response to stretch and high blood volume. Has opposing effect of aldosterone;
Dilate afferent and constrict efferent arteriole to increase GFR
Increase blood flow through vasa recta to wash out Na and urea
Decrease Na reabsorption in DCT

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4
Q

Define sepsis

A

SIRS + documented/presumed infection

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5
Q

Describe SIRS

A

Systemic inflammation, organ dysfunction and failure
On examination: pale, cold extremities, temperature, high HR and RR, low BP
Characterised by;
HR greater than 90
Resp rate greater than 20
WBC less than 4x10^9 or greater than 12x10^9
Temperature greater than 38 or less than 36

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6
Q

Where are peripheral and central chemoreceptors located?

A

Carotid and aortic bodies

Ventral surface of the medulla

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7
Q

What is the function of central chemoreceptors

A

Respond to changes in H+ concentration and CO2 in brain ECF
When local H+ rises central chemoreceptors stimulate the respiratory centre to increase ventilation
NB: CO2 can cross BBB but bicarbonate cannot as easily

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8
Q

What is the function of peripheral chemoreceptors

A

Respond to changes in O2, CO2 and pH.
In metabolic acidosis causes hyperventilation
In respiratory acidosis CSF pH is corrected quickly so stimulus for breathing relies entirely on peripheral chemoreceptors until renal compensation is complete (3-5 days)

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9
Q

What is the main action of ACE inhibitors?

A

Inhibit the conversion of angiotensin I to angiotensin II

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10
Q

What are the normal actions of angiotensin II

A

Causes aldosterone release from adrenal cortex
Vasoconstriction to increase blood pressure
Acts at NHE in PCT to stimulate Na reabsorption
Stimulate posterior pituitary to release ADH

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11
Q

Discuss the common side effects of ACE inhibitors

A

A persistent dry cough, thought to be as a result of increased bradykinin (angiotensin 2 normally breaks this down)
Cough caused by pro inflammatory mechanisms
Increased bradykinin may also cause angiooedema

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12
Q

Explain how hyperkalaemia may result from use of ACE inhibitors

A

ACE inhibitors reduce production of aldosterone. Normally aldosterone increases Na+ reabsorption and so K+ excretion. Reduced levels of aldosterone mean k+ may be retained

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13
Q

Describe afterload

A

Load that heart must eject blood against, related to aortic pressure and ventricular wall stress

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14
Q

In what situations will after load be increased

A

Aortic stenosis

High systemic vascular resistance

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15
Q

What changes as a result of increased afterload

A

Increased end systolic volume and decreased stroke volume

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16
Q

Define preload

A

Initial stretching of cardiac myocytes prior to contraction, related to sarcomere lengths

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17
Q

In what situations would you get increased preload

A

High CVP
High ventricular compliance
Low HR (increased ventricular filling time)

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18
Q

How do you work out CO

A

HR x SV

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19
Q

How do you calculate SV

A

EDV-ESV

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20
Q

How do you calculate BP

A

CO x TPR

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21
Q

What is EDV

A

Volume of blood in R/L ventricle at end if diastole just before systole

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22
Q

What is ESV

A

Volume of blood left in ventricle at end of systole

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23
Q

Define systolic pressure

A

Maximal pressure in aorta at end of contraction

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24
What is diastolic pressure
Minimal pressure in aorta occurring just before systole
25
What is the pulse pressure
Systolic pressure - diastolic pressure
26
What is the ejection fraction
Fraction of blood ejected by ventricle relative to EDV EF = SV/EDV -100
27
What is inotropy
Contractility.
28
Describe reactive hyperaemia
Transient increase in blood flow following a short period of ischaemia. When blood flow to an area is cut off temporarily, tissue hypoxia and vasodilator metabolises (adenosine) causes vasodilation and decreased vascular resistance. This means blood flow will be increased once restored
29
Give the 8 main stages of atheroma formation
1. Damage to endothelial lining of vessel 2. Causes LDL to accumulate in tunica intima 3. LDL becomes oxidised 4. Oxidised LDL attracts monocytes 5. Monocytes differentiate to macrophages which release cytokines attracting more monocytes 6. Macrophages phagocytise LDL to form foam cells 7. Macrophages stimulate collagen production to form a fibrous cap 8. Plaques calcify over time
30
What is the risk with an unstable plaque
Rupture may cause thrombosis from aggregation of platelets
31
When is atheroma clinically silent
Normal | Fatty streak
32
What may happen as a result of plaque rupture/thrombosis
MI Critical leg ischaemia Stroke Unstable angina
33
Describe a stable plaque
Small necrotic core, large fibrous cap
34
Describe an unstable plaque
Large necrotic core, thin fibrous cap
35
Give some non-modifiable risk factors for atherosclerosis
Age, being male, family history, genetic condition eg familial hypercholesterolaemia
36
Give some modifiable risk factors for atherosclerosis
Diet, weight, excercise, smoking, diabetes, vitamin b6 deficiency
37
Describe the action of statins
HMG-CoA Reductase inhibitors | Enzyme normally involved in cholesterol synthesis in the liver
38
What are the functions of VLDL
Carry triglycerides from liver to adipose tissue
39
What are the functions of LDL
Carry fat molecules around the body
40
What are the functions of HDL
Carry fat from adipose tissue to liver
41
What are the functions of Chylomicrons
Transport triglycerides from intestine to liver/muscle/adipose
42
Describe the posterior pituitary
Connected to hypothalamus by median eminence | ADH and oxytocin produced in hypothalamus and stored in posterior pituitary
43
Describe the results of over/under secretion of ADH
Over- SIADH | Under- diabetes insipidus
44
Describe the anterior pituitary
``` Glandular tissue, derived from Rathke's pouch Secrete strophic hormones eg Somatotrophs- GH Lactotrophs- prolactin Corticotrophs- ACTH Gonadotrophs- FSH and LH Thyrotrophs- TSH ```
45
How does the hypothalamus communicate with the anterior pituitary
Hypophyseal portal system
46
Describe the structure of haemoglobin
Tetra metric protein 4 sub groups, 2 alpha chains and 2 beta chains Each group has one haem molecule Each haem can bind 1xO2
47
Describe the structure of a RBC
No nucleus or mitochondria | Undergoes glycolysis for energy production
48
Describe cooperative binding
Once one O2 molecule is bound to Hb this promotes the presence of the R state, this makes it more easy for the next molecule of O2 to bind (conformational shift)
49
Describe the Bohr effect
In tissues where oxygen must be given up more quicker and readily eg muscle and placenta, the Bohr effect causes a shift to the right if the oxygen dissociation curve Caused by presence of: co2, H+, DPG and high temperature For any given pO2 Hb is less saturated
50
Describe HbF
Two alpha chains and two gamma chains | Much higher affinity for O2 then adult Hb ensure foetus gets all oxygen necessary. Shifts curve to left
51
Describe myoglobin
Exhibits hyperbolic binding Main store of oxygen in the body Can be released in muscle damage (rhabdomyolysis) and can cause acute kidney failure as it is nephrotoxic
52
Describe the use of HbA1C
Normal lifespan of an RBC is 120 days, glycosylation of rbc's in this time depends on the mean glucose level of blood over the previous 120 days. Therefore it is usually a reliable indicator of diabetic control over the previous 3 months
53
Where are alpha1 receptors found and what is their action
Arterioles (vasoconstriction) Bladder (sphincter contraction) Male sex organs (ejaculation)
54
Where are beta1 receptors found and what is their action
Heart (increase hr and force of contraction) | Kidney (increased renin release)
55
Where are beta2 receptors found and what is their action
Lungs (bronchodilation) Arterioles (vasodilation) Uterus (relaxation) Skeletal muscles/liver (glycogenolysis)
56
Where are m1 receptors found and what is their action (ACh)
Salivary glands- salivation | Stomach- acid secretion
57
Where are m2 receptors found and what is their action (ACh)
Heart- slow HR and reduce Contractility
58
Where are m3 receptors found and what is their action (ACh)
Smooth muscle- contraction | Lungs- bronchoconstriction
59
Describe the structure of neurones in the sympathetic NS
Thoracolumbar outflow T1-L2 | Short pre, long post-ganglion if neurone
60
Describe the structure of neurones in the parasympathetic NS
Craniosacral outflow S2-S4 | Long pre, short post-ganglionic neurone
61
Describe the action of beta-blockers
Beta adrenergic receptor antagonists. Block action of adrenaline at receptors therefore lowering HR and force of contraction. Also causes decreased renin secretion. Useful for treating hypertension, arrhythmia's and preventing second MI
62
Describe the action of calcium channel blockers
Work mostly at L-type voltage-gated sodium channels. By blocking the channels prevents influx of calcium, lowering HR, reducing Contractility of cardiac myocytes and causing vasodilation. Reduces afterload on heart and is often used to treat the pain of angina
63
Describe a STEMI
Heart muscle injured due to lack of oxygen, full thickness infraction shows ST elevation on ECG trace. May also show; pathological Q wave and T wave inversion.
64
Describe an NSTEMI
Partial thickness infarct does not show ST elevation, but ST depression and T wave inversion
65
Give 3 examples of cardiac biomarkers used
Cardiac troponins T and I Myoglobin Creatine kinase (CK-MB)
66
Describe the use of testing for cardiac troponins
T and I have both high specificity and sensitivity so are gold standard. Released specifically from cardiac myocytes on irreversible damage Levels increase within 3-12 hours of onset of symptoms, peak around 24-48 hours and return to baseline between 5-14 days
67
When would myoglobin be used as a cardiac marker
It is the fastest detectable marker that is most sensitive, it is released within 2 hours but has low specificity
68
Describe sensitivity and how it would be calculated
Ability to correctly diagnose a condition. If a patient has the condition, chance they will test positive for it TP/TP+FN
69
Describe specificity and how it would be calculated
Ability to correctly exclude a condition. If patient doesn't have condition, chance they will test negative for it TN / TN+FP
70
Describe PPV and how it would be calculated
If positive result, chance patient has disease | TP/TP+FP
71
Describe NPV and how it would be calculated
Proportion of negative results that are truly negative | TN/TN+FN
72
Give some prehepatic causes of portal hypertension
Portal vein thrombosis | Congenital atresia
73
Give some intrahepatic causes of portal hypertension
``` Cirrhosis Hepatic fibrosis Sarcoidosis Schistosomiasis Miliary TB ```
74
Give some posthepatic causes of portal hypertension
(Between liver and right heart) Hepatic vein thrombosis IVC thrombosis
75
Give the arterial supply and venous drainage of the liver
Arterial: hepatic artery (also portal vein brings blood from gut with nutrients) Drainage: hepatic vein
76
Give and explain some signs/symptoms of portal hypertension
Ascites: pressure backs up to abdomen, high hydrostatic pressure means less fluid reabsorbed, also may have hypoalbuminaemia Splenomegaly Portosystemic anastomoses: oesophageal, rectal Varices, caput medusae (peri umbilical vein)
77
Give some causes of pancreatitis
``` Gallstones Ethanol Trauma Scorpion bite Mumps Autoimmune Steroids Hypercalcaeima ERCP Drugs ```
78
Give some common cancers of the liver
Common for mets from GI Benign: hepatic Adenoma, haemangioma Malignant: hepatocellularcarcinoma, hepatoblastoma
79
Describe how the liver detoxifies
Hepatocytes/kuppfer cells deal with toxins | Toxins are excreted into the canaliculi then bile ductule then bile duct and will be eliminated by the gall bladder
80
Describe hepatic phase 1 metabolism
Makes toxins less fat soluble Via CYP450 Oxidation, reduction, hydrolysis, hydration
81
Describe hepatic phase 2 metabolism
Makes toxins more water soluble Conjugation pathways Sulfation, glucuronidation, glutathione, conjugation
82
Describe the actions of paracetamol
``` Inhibits COX (specifically cox-2) so prevents production of prstaglandins An analgesic and anti-pyretic ```
83
Describe the normal metabolism of paracetamol
Normally via phase 2 (90%) conjugation with surface and glucuronide 10% metabolism via phase 1 with CYP450. Produces NAPQI, toxic metabolite NAPQI then conjugated with glutathione before being renally excreted
84
Describe paracetamol toxicity
May have no symptoms for 24hrs Phase 2 saturated so undergoes phase 1 producing Napqi. NAPQI depletes glutathione and damages hepatocytes Give activated charcoal and n-acetylcysteine
85
Describe prehepatic jaundice
Unconjugated bilirubin May be due to increased production of bilirubin eg Gilbert's syndrome, excessive breakdown of RbC's eg g6pdh deficiency, thalassaemia, SCA
86
Describe hepatic jaundice
Mixed conjugated and unconjugated bilirubin | Caused by damage to liver: hepatitis, cirrhosis, alcohol, drugs
87
Describe post-hepatic/obstructive jaundice
Conjugated bilirubin Obstruction of bile duct, backs up to liver Pancreatic tumour, gallstones
88
Give some features of liver cirrhosis
``` Hyperammonaemia Encephalopathy Ascites Deranged clotting Palmar erythema Bruising Jaundice Anaemia Dupuytrens contracture ```
89
Describe the mechanism of developing fatty liver
Alcohol metabolism generates NADH from NAD+ High NADH leads to increased fatty acid synthesis Low NAD+ leads to decreased fatty acid oxidation, causing FA's to accumulate
90
Vaccines are available for hepatitis...
...A and B
91
Which nerve roots supply the biceps reflex
C5/6
92
Which nerve roots supply the brachioradialis/supinator reflex
C6
93
Which nerve roots supply the triceps reflex
C7
94
Which nerve roots supply the patellar reflex
L4
95
Which nerve roots supply the ankle reflex
S1