MCQ - Exam prep Flashcards
1
Q
What is the functional tissue of an organ called?
A
parenchyma - distinguid from the connective and supportive tissue
2
Q
What is sulphonylureas used for?
A
An anti-diabetic drug, widely used in the management of diabetes mellitus type 2
3
Q
The accumulation of cells, lipids and tissue in the intimal lining of arteries is what disease?
A
Atherosclerosis
4
Q
Structure of arteries and veins
Tunica Adventitia
Tunic Media
Tunica Intima
A
Adventitia -Strong and fibrous - holds vessel open
Media - smooth muscle and elastic - permits diameter changes
Intima - endothelium - lesions develop here
5
Q
Atherosclerosis - 5 Modifiable Risk factors
A
Obesity Hyperlipidaemia Smoking Diabetes (lifestyle related) Insufficient physical activity
6
Q
Atherosclerosis - 5 Non-modifiable risk factors
A
Age Premature menopause in females Indigenous Australian Low socioeconomic groups Family history of close relative with the disease under 60
7
Q
An autoimmune, neuromuscular disease caused by Ab-mediated loss of nicotinic ACh receptors at the NMJ
A
myasthenia gravis
8
Q
Myasthenic crisis symptoms
A
Severe muscle weakness -> Quadriplegia, SOB, Difficulty swallowing
Can occur 3-4 hours after too little or too much medication
Can be stress induced -> Infection, pregnancy, cold exposure, sugary
9
Q
Myasthnia gravis Tx
A
- Neostigmin & Pyridostigmine (Anticholinesterases)
- Corticosteroids
- Ciclosporin & Azathioprine (Immunosupressant)
10
Q
Bradykinesia
A
Slowness of movement
11
Q
Thiopentone (thiopental) - IV
A
- Induction Agent
- Enhances/mimics action of GABA in CNS by inhibiting excitatory neurotransmission.
- No analgesic effects
- Resp and CVS effects (depresses/decreases)
12
Q
GABA (Gamma aminobutyric acid)
A
- CNS inhibitory neurotransmitter
- Most widely distributed
- Reduces neuronal excitability in the nervous system
- Produced in presynaptic neurone and acts on postsynaptic GABA receptors.
13
Q
Propofol - IV
A
- Induction agent; suitable for maintenance and sedation
- Activates GABAa receptor
- Shortens opening time of nicotinic AChR and NA+ channels in cortex
- Rapid onset and fast recovery
- No analgesic properties
- Min CVS effects
14
Q
Ketamine - IV
A
- Induction agent; and maintenance
- NMDA rector antagonist (reduces neuronal excitability)
- Potent analgesic
- CVS stimulant
15
Q
Induction IV
A
- Thiopentone
- Propofol
- Ketamine
16
Q
What are some Inhalant anaesthesia agents?
A
‘flurane’
Sevoflurane
Desflurane
Isoflurane
fluranes are all volatile agents and can trigger Malignant Hyperthermia!
- Also N20 can be an induction and maintenance inhalant. No reversal for inhaled agents.
17
Q
Neuromuscular Blocking Agents (muscle relaxant) fall into which two categories?
A
Depolarising vs Non-depolarising
18
Q
Suffix -> aines are responsible for?
A
-Local anaesthsia
eg Lignocaine and Bupivacaine
-Block conduction of PNS impulses -> block sodium channels => no threshold potential
-Considerations for age, wt, health, liver function for dosage used.
19
Q
Bier’s block
A
Regional anaesthesia - local anaesthetic is given intravenously with a tourniquet applied to stop it from spreading systemically.
20
Q
Acute respiratory distress syndrome (ARDS)
Clinical presentation?
A
- Rapid onset (12-18 hours)
- ^ RR
- Metabolic acidosis
- Hypoxaemia refractory to O2 therapy
21
Q
What do drugs ending in ‘ole’ do?
A
Proton Pump Inhibitors (PPI) - Inhibit the formation of Hydrochloric acid
eg Pantoprazole, Omeprazole, Esomeprazole(Nexium)
Adverse effects - headache, dry mouth, GI upset (N,V,D)
22
Q
Cimetidine
A
- Histamine receptor antagonist - Used in Pyloric obstruction
- Blocks acid secretions
- Interacts with CYP -> metformin, warfarin etc
23
Q
Is Penicillin more effective against gram positive or gram negative bacteria?
A
Gram +++++++++++
24
Q
What is the mechanism of action of Penicillin?
A
Inhibits synthesis of bacterial cell wall - binds with proteins -> defective cell wall destroys the organism
Also called Beta-Lactam Antibacterials
25
Is Penicillin given IV or oral?
IV - as it is destroyed by gastric acid
26
What are some common Beta-Lactam Antibacterials?
Penicillins
Cephalosporins
Carbapenems
Monobactams
27
What are three common asthma medications
- Prednisolone
- Aminophylline
- Salbutamol
27
What are three common asthma medications
- Prednisolone
- Aminophylline
- Salbutamol
28
Stroke risk factors
- Smoking
- lifestyle (ethanol, obesity, cholesterol)
- HTN
- DM 1 & 2
- Heart disease
- Family Hx
- Chlamydia pneumonia
- ^Age
29
What is bioavailability of a drug?
Amount of active drug that reaches systemic circulation.
30
What affects the bioavailability of a drug?
Absorption
Intestinal motility
First pass hepatic metabolism
(IV = 100% bioavailability)
31
What are treatment options for genital herpes?
Antiviral agents - DNA polymerase inhibitors
- Aciclovir
- Famciclovir
- Valaciclovir (best)
32
What are Desflurane, Isoflurane and Sevoflurane used for?
Inhaled Induction agents
33
What are the 4 phases of wound healing?
1. Haemostasis (Immediate)
2. Inflammation (0-3 days)
3. Proliferation (2-24 days)
4. Maturation (24 days-1year)
34
What are the cells in the first stage of wound healing?
1. Haemostasis - Platelets are activated from exposed collagen and begin clotting. Platelets recruit Neutrophils (WBCs) and Monocytes(blood) to the site.
35
What are the cells in the second phase of wound healing?
2. Inflammation
Neutrophils and Macrophages phagocytosis bacteria and necrotic tissue. Macrophages release cytokines. Mast cells secrete histamine (causing vasodilation)
36
What are cells in the third stage of wound healing?
3. Proliferation
Fibroblasts produce the ExtraCellularMatrix(ECM) and collagen to form Granulation tissue as a framework. Macrophages continue to remove debris
37
What are cells in the fourth stage of wound healing?
4. Maturation
Fibroblasts continue to release a stronger and more organised collagen and create a stronger framework with 70-80% tensile strength recovered.
38
What are the three processes of wound healing?
Primary - Margins aligned
Secondary - left open, longer inflammation
Tertiary - Delayed primary, left open and closed later
39
What may cause wounds to become chronic?
Repeated trauma
Ischemia
Infection
40
What health conditions influence wound healing?
```
Diabetes
CVS conditions
Blood disorders (Anaemia)
Auto-immune disorders
Obesity or very thin
Stress
Phychiatric disorders
Medications
Smoking
```
41
What are the changes that age causes to skin?
- Dermis loses 80% thickness
- 40% Less collagen
- Less small blood vessels
- Epidermis and dermis seperate more easily
- Reduces sensory nerves
42
What is Suxamethonium used for?
IV, Depolarising NM Blocking agent aka Muscle relaxant for intubation.
Mimics the action of ACh -> agonist on nicotinic receptor on motor end plate DEPOLARISING +++ => Paralysis. Short acting ~5min
43
How do Non-depolarising agents work?
Act as a competitive antagonist to ACh at the nicotinic ACh receptor on NMJ to PREVENT DEPOLARISATION, Require reversal as they have CVS changes (decrease HR and BP)
44
What are medications ending in 'ium' used for? e.g Atracurium
Non-depolarising Neuromuscular Blocking Agent aka muscle relaxant.
Atracurium, Pancuronium, Rocuronium, Vecuronium.
45
What is the Loeser Model?
Pain model that puts the pain in context with biophysical and behaviour of pain.
Nocicoeption>Pain>Suffering>Pain behaviour
46
What are the 3 categories of Nociceptor pain receptors?
Mechanical receptor - myelinated
Thermal receptor - Myelinated
Polymodal receptor - Un-myelinated
47
What are the two different types of afferent nociceptors?
Myelinated - Delta - Fast 30m/sec
| Un-myelinated - C - Slow 12m/sec
48
What are 2 neurotransmitters involved in pain transmission?
Substance P - send signal to higher brain areas, opioids block this.
Glutamate
49
What is angina?
Reversible myocardial ischaemia
| -Caused from increase in myocardial O2 demand eg stress and exercise
50
What is Prinzmetal angina?
Coronary spasm, reversible myocardial ischaemia that happens at random, usually at night. Pathology unclear, possibly altered Ca+ channels
51
What is unstable angina?
Unpredicatable, no clear cause from stress etc.
| Intermediate b/t stable angina and MI
52
What are diagnostic tests for angina Sx?
Hx, vitals, ECG, CXR, Blood test, Echocardiogram, Angiogram, exercise stress test.
53
What are 4 pharmacological management options for unstable angina?
O2, GTN, Aspirin, Morphine
54
What are 'olol's used for?
```
Beta blockers! for stabel angina
-Decrease HR,
-Decrease force of contraction
= decrease BP
Adverse effects are Brady cardia and orthostatic HTN
```
55
What are 'pril's used for?
ACE Inhibitors! Inhibit Angiotensin Converting enzyme, which prevents Angiotensin I converting to Angiotensin II. Leading to reduced peripheral resistance,
56
What is the term for incomplete or partial paralysis?
Paresis
57
What does Hemiparesis mean?
Incomplete paralysis affecting one side of the body
58
What does Hemiplegia mean?
Paralysis of one side of the body
59
What is the term for the loss of the ability to speak or write?
Aphasia
60
What does Apraxia mean?
Inability to execute motor acts
61
What is the term for poorly articulated speech?
Dysarthria
62
What is Dysphagia?
Difficulty swallowing
63
What is Agnosia?
loss of recognition ability; people or shapes
64
What is Hemianopia?
Blindness in half the field of vision
65
What is Cerebral Blood Flow mainly regulated by?
In response to changes in O2, H+ and CO2
66
What is Cerebrovascular Disease?
A neurological disorder defined as the abnormality of the brain, caused by a pathological process in the blood vessels.
67
What is a common clinical manifestation of CVD?
Stroke (Cerebrovascular accident)
68
What are the risk factors for Stroke?
- Smoking.
- Lifestyle (Obesity, cholesterol)
- HTN
- Type 1&2 DM
- Heart disease eg AF
- Hx or Family Hx of stroke
- Chlamydia pneumonia
- Age
- Gender - higher in Men
69
What are four types of Ischemic Stroke?
- TIA (Transient ischaemic attack), temporary and intermittent blockages.
- Thrombotic stoke, artery occlusion from thrombus in cerebral arteries.
- Embolic stroke, fragments from outside the brain.
- Lacunar stroke, micro-infants in smaller arteries
70
What is an area of irreversibly damaged tissue called?
Infarct
71
What is Type I Acute Respiratory failure classified as?
Hypoxaemia with normal CO2
| Reduced O2 in the blood
72
What is Type II Acute Respiratory Failure
Hypoxaemia and Hypercapnia
| Reduced blood O2 and increased blood CO2
73
COPD Patients should aim to have SpO2 between what %?
88-92% to allow effective CO2 removal. If over-titrating supplemental O2, can cause impact on the transportation and removal of CO2
74
What is the main cause of Acute Pulmonary Oedema (APO)?
Cardiogenic causes related to an increase in Left Atrial Pressure. Leads to increase pulmonary hydrostatic pressure -> oncotic pressure ->fluid moves into interstitial space that exceeds lymphatic drainage.
75
What is the mechanism of action of Frusemide? And some adverse effects?
Its a diuretic. It inhibits the reabsorption of Na+ and Cl- in the ascending limb of loop of Henle. This results in less water being reabsorpted => more water excreted.
Adverse effects are electrolyte disturbance, polyuria, orthostatic hypotension. Hyponatraemia and hypokalaemia
76
What is Atelectasis? and what are the common causes?
Collapse of lung tissue. Can be caused by:
- Pleural effusion
- Any surgery
- Blocked airway
- Respiratory distress syndrome
77
What is Acute Respiratory Distress Syndrome (ARDS)?
Damage to capillary/alveolar membrane resulting in leaking of fluid into alveolar space. Massive inflammatory response - Synthesis and release of inflammatory mediators: Neutrophils, macrophages, endotoxin, IL-1, TNF, ROS.
Leads to pulmonary oedema+++
78
What is the most common cause of respiratory failure in children?
Respiratory distress syndrome - due to lack of surfactant leading to alveolar collapse.
79
What are risk factors for pneumonia?
- Age
- Immunocompromised
- Underlying pulmonary disease (COPD, asthma)
- Alcohol, smoking
- Prolong immobilisation
80
Where are Beta 2 receptors located? and what does a secondary messenger do when activated by medication?
Located mainly in the lungs (Some in heart (mainly B1)). Drugs like salbutamol and salmeterol stimulate Beta 2-adrenergic receptors causing relaxation of bronchial smooth muscle. The receptors have a secondary messenger system of increasing the production of cyclic AMP (cAMP) which also produces bronchodilation.
