questions Flashcards

1
Q

explain how liver cirrhosis can lead to portal hypertension? 6

A

1.) Liver cirrhosis causes liver tissue to become fibrous and rigid/hardened
2.) This disrupts the blood flow through the liver
Blood begins to backflow to the Portal Vein
3.)Blood accumulates and causes an increase in pressure — portal =hypertension
4. Blood continues backflowing to the collateral blood vessels in the upper GI tract and rectum/anus
5. Weak blood vessels — dilate and twist , become varicose veins
6. Eventually rupture due to the increased pressure — leading to bleeding

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2
Q

Explain how gallstones can lead to pancreatitis? 6

A
  • Gallstone is squeezed out of the gallbladder with the bile after patient eats
  • Blocks the sphincter of Oddi — bile is blocked
  • Bile backflows into the pancreatic duct
  • Presence of bile activates proteases — such as Trypsinogen — that are present in the pancreas
  • These start to auto digest the pancreatic tissue
  • Inflammatory response — Pancreatitis
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3
Q

• Explain how gallstones can lead to fatty stools?
• How can they also lead to pain in the upper right quadrant of the
abdomen?
5

A
  • Block the sphincter of Oddi
  • Bile cannot enter intestines — bile normally helps to break down fats - therefore absence of bile means fats go undigested through the intestines ; Lipase enzyme
  • Undigested fats excreted with the stool
  • Gallstones are sharp — scratch the common bile duct wall as they pass through — causing local injury
  • Localized stimulation of nociceptors due to injury — pain response
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4
Q
  • Explain first pass effect/metabolism of a drug?

* Which route of administration avoids the first pass effect? 2

A
  • Part of the drug is metabolized by the liver before it reaches the systemic circulation, therefore reducing the bioavailability of the drug.
  • Intravenous route as it enters the systemic circulation immediately
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5
Q

Define asthma 2

A
  • A chronic inflammatory disease of the bronchioles

* Hypersensitivity of the bronchioles which results in bronchospasm

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6
Q

• Chloe is asthmatic, she has been prescribed a salbutamol inhaler.
Explain the mechanism of salbutamol, and how this will help her
symptoms of asthma?
4

A
  • Salbutamol is an agonist of Adrenaline
  • Binds to B2 receptors on the smooth muscle cells of the bronchioles
  • Causes sympathetic stimulation — results in bronchodilation
  • Therefore, dilated airways will reduce the symptoms of asthma
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7
Q

• Another drug that can be used is Ipratropium Bromide, explain the mechanism of this drug. 3

A
  • Ipratropium Bromide is an antagonist of Acetylcholine
  • It blocks the muscarinic receptors on the smooth muscle cells of the bronchioles
  • Therefore, it inhibits Acetylcholine from binding and therefore stops bronchoconstriction from occurring
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8
Q

• Why do asthma sufferers have worse symptoms on exhalation? 3

A
  • On exhalation, pressure in the airways naturally decreases
  • This causes passive narrowing of the airways
  • In asthma, the airway is already narrow, further narrowing of the airway on exhalation will cause worse symptoms
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9
Q

• Greg suffers from MS and neuropathic pain as a consequence. Explain
what Neuropathic pain is and how MS causes this? 4

A
  • Neuropathic pain is pain that is felt from a normally non — painful stimuli
  • MS causes demyelination of axons/damage and destruction to the myelin sheath
  • This causes the neuron to become irritated
  • A spontaneous action potential is created, if this occurs on a sensory neuron, the action potential is perceived as a pain message.
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10
Q

explain the pain pathway 6

A

• Localised injury stimulates local nociceptors = Transduction
• ISt order neuron — spinal cord
• 2nd order neuron — thalamus in the brain
• 3rd order neuron — somatosensory cortex of the brain
=Transmission
• PAG layer = perception of pain
• Finally, modulation of pain occurs — different in everybody, how the
body deals with the pain.

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11
Q

• Explain how opiates, such as Morphine, work to reduce pain? 8

A
  • Bind to opiate receptors on the pre-synaptic membrane
  • Stop calcium influx by closing the calcium ion channels
  • Therefore no/very little neurotransmitter is released into the synaptic cleft
  • Action potential (pain message) will be unable to be transmitted across.
  • Also bind to opiate receptors on the post-synaptic membrane
  • Cause the membrane to become hyperpolarized
  • Hyperpolarized membrane is unable to generate an action potential
  • Therefore pain messages will not be received, pain will be reduced.
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12
Q

• When a localized injury occurs, the symptoms of inflammation are
seen. Explain what these symptoms are and how they are caused?
5

A

•Localised injury activates Mast cells
•These release Histamine and Prostaglandins
Localized vasodilation occurs — increases blood flow to the area= Causing redness and heat
•Increased vascular permeability
• Fluid leaks into the localized area and accumulates—Causing swelling/oedema
•Presence of fluid stimulates local pain receptors—Causing pain

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13
Q

• NSAID’s such as ibuprofen can be used to reduce inflammation,
explain their mechanism of action. 4

A
  • NSAID’s inhibit COX enzymes
  • These enzymes increase prostaglandin productions, therefore when they are inhibited, prostaglandin production decreases
  • Less prostaglandins reduces the strength of the inflammatoryresponse
  • Therefore, causing a reduction:in the symptoms.
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14
Q

• Grace has been in a car accident and has lost a lot of blood.
• Her observations are
• HR 130
• RR 28
• BP 105/65
• Explain the physiological mechanisms behind the observations seen.
13

A
  • As Grace has lost a lot of blood volume, her compensatory mechanisms are causing her observations.
  • When her BP was falling, the baroreceptors — located in the aortic arch and carotid sinus — would have detected this.
  • An afferent message would have been sent to the CCC in the medulla oblongata of the brain
  • Then an efferent message would have been sent to the SA node to increase the firing rate
  • Increased firing rate from the SA node = increased HR
  • This is to try and maintain the blood pressure, and adequate circulatory flow around the body
  • The loss of blood volume would also mean that there would be inadequate oxygen delivery to tissues.
  • Cells would begin to respire anaerobically, causing Lactic Acid to be produced.
  • This would lower the pH of the blood — detected by chemoreceptors.
  • An afferent message would be sent to the RCC in the medulla oblongata of the brain
  • An efferent would then be sent to the diaphragm and external intercostal muscles.
  • Increased sympathetic stimulation — increase frequency and strength of contractions
  • Causing an increased respiratory rate
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15
Q

• What type of shock is Grace suffering from?
• If her shock progresses, what would the hallmark symptom be to
diagnose this?
2

A

• Hypovolemic / hemorrhagic
• Hypotension with tachycardiac — as this would show failure of those
compensatory mechanisms

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16
Q

• Grace’s blood type is AB-, she needs a blood transfusion.
• What blood types can she be given?
3

A
• AB can receive all 4 —A, B, AB, and O
• However Rhesus negative can only be given negative blood
• Therefore she can be given
-A-
B-
AB-
O-
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17
Q

• What is hypoxia?
• What are the 4 types of hypoxia?
5

A
  • A state in which the body is deprived of adequate oxygen supply at tissue level
  • Hypoxic
  • Anaemic
  • Stagnant
  • Histotoxic
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18
Q

• Define dementia
• What are the 3 types?
4

A
  • A term to describe conditions that include a decline in memory and reduction in ability to do daily activities
  • Alzheimer’s
  • Frontotemporal
  • Vascular
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19
Q

• What are the two types of hormones and what are their differences?
6

A
Peptide
- Water soluble
- Bind to receptor on the surface of the cell
 Steroid
- Lipid soluble
- Bind to receptor inside the cell
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20
Q

• Explain the fight or flight system, including the hormones involved? 8

A
  • Acute stress stimulus
  • Adrenaline and noradrenaline released from adrenal glands
  • Sympathetic stimulation
  • Increased HR and RR
  • Dilated pupils
  • Muscle tremors
  • Eventually, noradrenaline causes parasympathetic stimulation
  • Reverse of symptoms
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21
Q

• Explain how calcium levels are increased if they are too low?
4

A
  • Parathyroid hormone released from parathyroid gland
  • Increases activity of osteoclasts — more calcium released into body
  • More calcium absorbed from intestines
  • Stop calcium being excreted by kidneys
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22
Q

• Explain how blood glucose levels are reduced? 2

A

• Insulin released from Beta cells of the pancreas
Encourages uptake of glucose into target cells
• Promotes blood glucose to be converted into glycogen stores

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23
Q

• Explain how blood pressure is increased by the RAAS? renin aldosterone angiotensin system

11

A
  • LOW BP detected by kidneys — Renin released
  • Liver releases Angiotensinogen
  • Renin + Angiotensinogen = Angiotensin 1
  • Lungs release ACE (Angiotensin converting enzyme)
  • Catalyzes the production of Angiotensin 2
  • Angiotensin 2 directly causes vasoconstriction = increased SVR
  • Stimulates release of Aldosterone from Adrenal Gland
  • Increases sodium reabsorption at the distal convoluted tubule of the nephron
  • Water follows sodium into the blood due to osmotic changes
  • Increased blood volume increased CO
  • Increase CO and SVR will increase blood pressure
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24
Q

• Explain the mechanism of ADH 6

A
  • Released by pituitary gland in response to low
  • Works on collecting duct of nephron
  • Increases amount of aquaporin channels
  • Water moves passively into blood
  • Increase blood volume = Increase CO
  • Increase BP
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25
Q
  1. Which of the following statement is correct about the mechanism of action of
    antibiotics:
    (1 mark)
A
  • Penicillin inhibits peptidoglycan synthesis
  • Streptomycin inhibits protein synthesis
  • Metronidazole inhibits DNA synthesis
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26
Q

TRUE OR FALSE
Asthma is a chronic disorder Of the alveoli
Pneumonia is an acute infection Of the bronchi
Bronchitis is an inflammation Of bronchioles

A

ALL FALSE

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27
Q

First pass metabolism may reduce drugs bioavailability, Which organ is involved in
‘First pass metabolism’ of a drug:

A

LIVER

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28
Q

What substances normally found in the blood are not normally found in urine?

A

PROTEINS

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29
Q

Which is the correct formula for blood pressure?

A

BP=COXSVR

30
Q

Which of the following effects of calcium channel blockers causes a reduction in
pressure?

A

Decreased systemic vascular resistanCE

31
Q
Angiotensin 11 produced in response to a fall in BP will...
Stimulate sodium retention
Increase blood volume
Stimulate thirst
Cause vasoconstrictipn
All of the above
A

ALL OF THE ABOVE

32
Q

Patients with chronic bronchitis produce large amount of sputum (mucus) in their
airways. Which type of cells produce mucus in the airways?
(1 mark)

A

GOBLET CELLS

33
Q
The innate immune response is the body's first line of defence against infection.
Which of the following options is not part of the innate immune response?
Activated B cells producing antibodies
Inflammatory response
Activation of complement system
Vomiting
Fever
Mast cells
Blood clotting
A

Activated B cells producing antibodies

34
Q
  1. Which immune cell is responsible for the release of histamine and prostaglandins that
    causes the signs and symptoms with inflammatory response?
    (1 mark)
    Lymphocytes
    Mast cells
    Neutrophils
    Macrophages
A

MAST CELLS

35
Q
  1. Bacterial cell walls have different structural properties which are classified into
    Gram positive and Gram negative bactekia. Gram-negative bacteria have:
    (1 mark)
    A. a thick peptidoglycan cell wall
    B. a thin peptidoglycan cell wall
    C. a thin layer of peptidoglycan sandwiched between two cell membranes I
    D. no cell wall
A

C. a thin layer of peptidoglycan sandwiched between two cell membranes

36
Q
  1. Which of the following statement is correct about aspirin:
    It inhibits clotting factor X
    It inhibits platelet aggregation
    It stimulates plasmin that turns fibrinogen into fibrin
    It changes prothrombin into thrombin
A

It inhibits platelet aggregation

37
Q
The two main types of sensory receptors that provide input to the cardiovascular
centre are:
(1 mark)
A. Baroreceptors and Mechanoreceptors
B. Baroreceptors and Properioreceptors
C. Baroreceptors and Chemoreceptors
D. Chemoreceptors and Osmoreceptors
A

C. Baroreceptors and Chemoreceptors

38
Q
Which of the following mechanisms prevents blood loss?
Vascular spasm
Platelet plug formation
Blood coagulation
All of these
None of these
A

all of these

39
Q

. Insulin is a hormone released by beta cells of the pancreas in response to
hyperglycaemia. Insulin:
(1 mark)
Decreases the uptake of glucose by muscle cells
Decreases the uptake and utilisation of glucose by most nerve cells
Increases the uptake and utilisation of glucose by muscle cells and liver cells
A and B are correct

A

Increases the uptake and utilisation of glucose by muscle cells and liver cells

40
Q

The term lung compliance refers to:
A. The cohesion of respiratory and muscle tissue
(1 mark)
B. The required air volume that must be forced out of lungs during expiration
C. The ease in which the lungs and thoracic wall can be expanded
D. Defaulted breathing which is characteristic of asthmatic individuals

A

The ease in which the lungs and thoracic wall can be expanded

41
Q
  1. Which of the following statements are correct about Aspirin:
It has an anti-inflammatory effect
It inhibits platelet plug formation
It has an anti-pyretic effect
All of the above
Only A and b are correct
A

all of the above

42
Q

Define Shock

A

A clinical state in which the organs and tissues do not receive adequate blood flow to meet their metabolic needs.

43
Q

Explain the mechanism of action of loop diuretics such as Furosemide.
3

A

-Diuretics are substances which elicit diuresis (increase in urine output).
-Furosemide inhibits tubular sodium reabsorption (Na+-K+-CI- co-transporter) from ascending loop of henIe (1 mark).
- Consequently, water stays with sodium
in the nephron leading to an increase in urine production (1 mark).

44
Q

C. Scott’s breathing becomes very difficult and start to have asthma attack. He takes
his spray, which contains Ipratropium Bromide. Explain in detail the mechanism
of action of Ipratropium Bromide.
(3 marks)

A

Ipratropium Bromide is an anti-muscarinic drug (or an antagonist drug)
(1 mark)
It blocks Acetylcholine (Ach) neurotransmitters attach to its muscarinic
receptors (1 mark)
on the smooth muscles of the bronchioles and causes bronchodilation (1 mark)

45
Q

D. Explain why Scott’s skin is pale, cold and clammy?

2 marks

A

Due to dehydration and low BP, (1) the peripheral blood vessels constrict by sympathetic nervous system to divert the blood from non-vital organs to the vital
organs. Therefore, less blood goes to skin and digestive system. The skin becomes
cold and clammy (1).

46
Q

A. What is bronchitis?

1 mark

A

inflammation of bronchi which leads to too much mucus production and
cough (don’t accept bronchioles)

47
Q

Explain how will bronchitis causes the following observations?

  • Wheezing
  • Low oxygen saturation
  • Bluish tinge
  • Confusion
A

Wheeze- sound of air forcing its way through restricted airway
Oxygen saturation of 90%- reduced gas exchange= less 02
into blood due to restricted airways•» less 02 available to bind to Haemoglobin (HÄ)
Bluish tinge- cyanosis due to reduced oxygen saturation.
Oxygenated blood has a red tinge, deoxygenated has bluish tinge
Confused- due to inadequate 02 supply to brain

48
Q
  1. Georgina is taking ACE inhibitors to control her hypertension. Explain the mechanism
    of action of ACE inhibitors in lowering her BP.
A

ACE enzyme converts Angiotensin I to Angiotensin 11 (1 mark)
(4 marks)
Angiotensin 11 is potent vasoconstrictor and increases SVR (1 mark)
It also stimulates aldosterone release from adrenal glands to increase Na+ and water reabsorption from distal convoluted tubules of nephron hence to
increase blood volume…(l mark) > increase venous return…> increase Cardiac output
ACE inhibitors block action of this enzyme, hence, absence of Angiotensin II reduces blood pressure.
(1 mark)

49
Q

What fluid flows in cystic duct? What fluid flows in common bile duct? What fluid
flows in pancreatic duct? What fluid passes through sphincter of Oddi? (2 marks)

A

Bile and Pancreatic juice

50
Q
  1. Explain how gallstones could lead to acute pancreatitis?l
    (3 marks)
A

Gallstones may move out of gallbladder and block the sphincter of Oddi, therefore blocking the entry of bile and pancreatic juice into the duodenum (1 mark)

This blockage leads to build up of pressure and back flow of bile and pancreatic juice into pancreas and activation of proteinases (proteases) in the pancreatic tissue (1 mark).
Activated proteinases causes auto-digestion of structural proteins in the pancreatic tissue which leads to pancreatitis (1 mark)

51
Q
  1. What is cirrhosis? Explain how it could potentially lead to upper Gl bleeding?
    (4 marks)
A

Cirrhosis is a condition of the liver characterized by the formation of scar tissue (fibrous tissue). The scar tissue will restrict the blood flow through the liver and interfere with the normal liver’s function (1 mark)

Cirrhosis restricts blood flow through the liver which leads to portal hypertension (1 mark)

This leads to back flow of blood to collateral blood vessels supplying blood to portal
vein including the small blood vessels around the lower part of oesophagus (1 mark).

The increased pressure in smaller collateral vessels make them bulged and twisted
(called Oesophageal varicose) which could potentially rupture and lead to bleeding (1
mark).

52
Q

What is angina and what causes it?

2

A

Angina is the chest pain occurs when blood supply to myocardium restricted Caused by atherosclerosis/fatty deposit in coronary blood vessels that reduces blood flow to the heart muscle (1 mark).
Cells go through anaerobic respiration with leads to lactic acid production.
This stimulate pain receptors, lead to angina (1 mark).

53
Q

Explain how drugs such as GTN relives angina?

Glyceryl trinitate 4

A

GTN absorbed directly into the system circulation by-passing first pass metabolism. It stimulates endothelial cells of the coronary arteries and other
blood vessels to produce nitric oxide (1 mark).

Nitric oxide diffuses to smooth muscle cells of blood vessels and causes smooth muscle relaxation or vasodilation (1 mark).

Vasodilation in coronary arteries improve blood flow/oxygenation to the cardiac muscles and therefore
no more anaerobic respiration (1 mark).

G TN also reduces pre-load and after-load. This will reduces the work of the heart and reduction in oxygen demand by the heart (1 mark)

54
Q

An agonist..

A

Mimics a chemical messenger causing an effect produced in the cell

55
Q

Salbutamol is .

A

A sympathomimetic drug, attached to Beta 2 adrenergic receptors
causing bronchodilation

56
Q

Angiotensin Converting Enzyme (ACE) works in the
of the active form of Angiotensinogen known as:
(1 mark)

A

angiotensin 11

57
Q
  1. Explain how salbutamol causes side effects such as tachycardia and muscle
    tremor. (2 marks)
A

Salbutamol is an agonist drug, mimics the action of adrenaline. It attaches to beta-I recéptors on SA node cardiac muscles generating faster action
potential which leads to increased heart rate (1 mark).

Another mark for Muscle tremor- Salbutamol attaches to Beta-2 receptors on skeletal muscles and causes tremor (1 mark).

58
Q
  1. Name two chemicals required for digestion of lipids in our food. State their
    mechanism of action.
    (2 marks)
A

Bile from liver/gallbladder- Mechanical digestion (increase the surface area for
lipase enzyme to work) (1 mark)

Lipase from pancreas- Chemical digestion- break lipids into smallest units to be absorbed (fatty acids and glycerol) (1 mark)

59
Q
  1. Explain how an epidural administration of Bupivacaine can anaesthetise the
    lower part of the body?
    (2 marks)
A

Bupivacaine is a sodium channel blocker, that prevents action potential generation or propagation as a result the pain messages will not reach the brain.

60
Q
  1. Explain the difference between epidural and spinal administration of
    Bupivacaine.
    (1 mark)
A

in the spinal canal, but outside the dura, slower but safer than spinal where the injection is placed under the dura in the subarachnoid space

61
Q
  1. Explain the mechanism of action of morphine as a potent analgesic. (3 marks)
A

Morphine attaches to opioid receptors at pre-synaptic membrane, prevents calcium into axon terminal Hence no signal to release neurotransmitters into the synapse.

Therefore, no pain signal transmission to the receiving neurone

Morphine is attached to opioid receptors on post-synaptic membrane and hyperpolarises the membrane. Therefore it is harder to be stimulated.

62
Q
  1. Explain how opioids such as Morphine causes nausea and vomiting. Name an
    anti-emetic drug and briefly explain its mechanism of action.
    (3 marks)
A

Metoclopramide (1 mark), It is an antagonist. It blocks D2 Dopamine receptors (1 mark) in the Chemoreceptor trigger zone in the brain (1 mark).

63
Q
39. Which of these is not an early symptom of shock?
Hypotension
A.
Tachycardia
B.
Tachypnoeic
c.
Altered mental state
D.
A

hypotension

64
Q

What causes neurogenic shock?

A

Trauma or injury to the head or spinal cord leading to loss of sympathetic stimulation
including Loss of tonicity of blood vessels

65
Q

circulatory system

A
r atrium 
r ventricle
pulmonary artery
lungs 
pulmonary vein 
l atrium 
l ventricle
aorta
body
venacava
66
Q

compare Dep MS to non dep MS

A

`DMS act as a acetylcholine receptor agonist

NDMR is a competitive antagonist

67
Q

GTN

A

vasodilating agent

68
Q

bacteriostatic vs bactiroscidal

A

static- prevents growth penicilin

cidal- kills tetracycline

69
Q

explain mechanism of antibiots

A

inhibition of cell wall synthisis
inhibitionof protein synthesis
alteration of cell membranes
inhibition of nucleic acid synthesis

70
Q

gram negative and gram positive bacterial cell wall structure

A

+ purple stain
thick peptidoglycan layer
multipla peptidoglycan layers

  • pink stain
    thing pepti layer
    single pepti layer
71
Q

chrons and ulcerative chrons

A

appears anywhere in gi tract
patchy pattern of inflammation

ulcerative - only appears in teh colon
continuous oattern fo inflammaton