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MD2002 > Random Question Generator for Revision MSA > Flashcards

Random Question Generator for Revision MSA Flashcards

1
Q

What are the chemical barriers to infection belonging to the innate immune response

A

-Fatty Acids on skin
-Low pH of stomach
-Secretion of antibacterial peptides like defensins (in gut and skin) and cryptidins ( in gut)

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2
Q

What are the mechanical barriers to infection belonging to the innate immune response?

A

-Air and fluid flow across epithelium
-Movement of mucus by cilia
-Tight junctions between cells

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3
Q

What compounds are present in eosinophils granules?

A

-Histamines, RNases, DNases, peroxide, Major Basic Protein, lipase and plasminogen

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4
Q

What are Gap junctions?
What’s their structure?

A

Site of low electrical resistance that electrically links cardiomyocytes(allowing diffusion of ions) so they contract simultaneously.
They are composed of 6 connexons subunits

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5
Q

What is the role of junctions in smooth muscle structure

A

Gap junctions electrically links cells
Focal adhesions structurally links cells

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6
Q

Describe muscle development

A

Embryonic mesoderm cells called myoblasts proliferate and enlarge.
Myoblasts then fuse together forming myotube.
Myotube matures and becomes a skeletal muscle fiber

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7
Q

Name and describe the supporting proteins of sarcomere

A

Alpha actinin- maintains actin in place attaching it to Z disks
Titin- Involved in recoil of muscle
Nebulin- provides structural and regulatory support to actin
Dystrophin- maintains integrity of muscle. Stabilizes muscle during contraction to avoid injury or damage

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8
Q

Describe structure of myosin

A

Made up of:
- 2 interwined chains of MHC
-2 light chains of MLC-1 that sustain myosin head
-2 light chains of MLC-2 that regulates ATPase activity of myosin

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9
Q

Describe the process of Calcium release for contraction

A

-When depolarisation travel down T tubules, the DHPR located in the T tubules membrane changes conformation and associates with the Ryanodine receptor of the SR.

-The Ryanodine receptor opens, allowing outflow of calcium ions out of the Sarcoplasmic Reticulum.

-Calcium ions then bind to TnC which will expose the actin-myosin binding sites.

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10
Q

Describe the properties of SERCA
What is the role of calsequestrin in muscle relaxation

A

SERCA is Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase. It pumps intracellular calcium ions back into the Sarcoplasmic reticulum after contraction of muscle. 2 Ca 2+ in SR per ATP.

Calsequestrin binds to Calcium ions at high concentrations and releases it at low intracellular concentrations. It acts as a calcium store during relaxation. It binds to 43 Calcium ions per molecule of calsequestrin.

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11
Q

Aside from SERCA and Calsequestrin what other proteins are involved in cardiac muscle relaxation.

A

Calcium-Sodium exchanger- Pumps 3 Na+ into cell for every 1 Ca2+ out.
Na+/K+ pump which brings the cell to resting potential, preventing the unwanted depolarisation of cell after so much Na+ is pumped in.

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12
Q

Name the roots that supply each terminal nerve

A

Musculocutaneous nerve- C5,C7
Axillary nerve-C5,C6
Median nerve-C6-T1
Radial nerve- C5-T1
Ulnar nerve C7-T1

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13
Q

Formation of creatinine phosphate
How does creatine phosphate provide ATP?

A

-ATP+ creatinine= Creatine phophate+ ADP

-Creatine Phosphate+ ADP= creatinine kinase= creatine +ATP
Craetine phosphate has a slightly higher energy level than ATP, so it gives off phophate groups more readily

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14
Q

Muscle fibre types and properties

A

-Slow Oxidative(Type Ia fibres): slow myosin ATPase activity, high oxidative capacity
-Fast oxidative-glycolytic(Type IIa) fibres: fast mATPase activity, intermediate, high oxidative capacity, intermediate glycolytic capacity
-Fast-glycolytic(type IIb/IIx fibres): fasr myosin ATPase activity, fast glycolytic capacity

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15
Q

Difference muscle tension and load

A

Muscle tension- force exerted by a contracting muscle
Load- force exerted by an object to be moved

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16
Q

Regulating factors of smooth muscle contraction

A

-Spontaneous electrical activity from pacemaker cells
-Ion concentration
-Acidity
-Stretch
-Hormones

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17
Q

4 muscles of pectoral region and their innervation

A

-Subclavius- innervated by subclavius nerve( C5 and C6)

-Pectoralis Major- innervated by median pectoral nerve (C8, T1) and lateral pectoral nerve(C5,C6,C7)

-Pectoralis minor- innervated by median pectoral nerve (C8,T1)

-Serratus anterior- innervated by Long thoracic nerve( C5,C6,C7)

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18
Q

Function of the 4 muscles of pectoral region

A

-Subclavius- moves clavicle
-Pectoralis major- moves humerus
-Pectoralis minor and serratus anterior- move scapula

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19
Q

What drugs can inhibit ACh release?

A

-Local Anesthetics
-Calcium inhibitors like Magnesium ions and antibiotics that bind to calcium like gentrimicin and tetracycline
-Neurotoxins like botulinum toxin and beta-bungarotoxin.

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20
Q

When can NMJ blocking drugs be used?

A

-Endotracheal intubation
-During operative procedures to ensure immobility- general anaesthetics
-In intensive care when patient placed on mechanical ventilator
-in electroconvulsive therapy

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21
Q

Action of non-depolarising blockers and example

A

They are AChR antagonists
-Binds to ACh receptors causing it to remain closed. ACh can’t bind
-Decreases the End Plate potential
-Decrease the depolarisation of motor end plate region
-No action potential generated in muscle as threshold not reached

Examples: atracurium(medium onset, medium duration), rocurorium( fast onset, medium duration)

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22
Q

Action of depolarising blockers and example

A

They are AChr agonists
-Binds to ACh receptor, triggering influx of Na+ and allowing depolarisation
-Persistent depolarisation of motor end plate
-Prolonged End Plate Potential and depolarisation of muscle
-Membrane reaches threshold
-Sodium channels remain refractory- electrically inactive
-More action potentials can’t be generated.

Example: suxamethonium( fast onset, slow duration)

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23
Q

Name the NMJ depolarising drugs, their onset and duration.
Which of these are aminosteroidal, and which are benzylisoquiolinium?

A

Pancuronium: medium, long
Vecuronium;medium, medium
Rocurorium: fast, medium
Atracurium: medium,medium
Mivacurium: Fast, short
Suxamethonium: Fast, short

P,V,R are aminosteroidal. A and M are benzylisoquiolinium

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24
Q

What can kinetic energy be transformed into?

A

Light, chemical, sound and heat energies

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25
Q

What can potential energy be transformed into?

A

Chemical, gravitational, nuclear and mechanical energies

26
Q

Describe the process of Electron Transport Chain

A
  • NADH delivers electrons into complex I while FADH2 delivers electrons into complex II
  • Complexes get reduced then oxidised.
  • Energy produced used to pump H+ into intermembranous space of mitochondria setting an electrochemical gradient.
  • Coenzyme Q delivers electrons from Complex I and II into complex III.
  • Cytochrome c delivers electrons from complex III into complex IV.
  • Complex IV combines 2H+O2 to form water.

-Complex V is ATP synthase. Only way H + can re enter matrix through , so they pass complex V, generating enough energy for ATP to be produced.

27
Q

Enzymes in the Respiratory Chain

A

In complex I NADH-Q reductase= Oxidises NADH +H+ and reduces coenzyme Q.

In complex II, succinate-Q reductase= Oxidises FADH2 and reduces coenzyme Q.

In complex III, Q-cytochrome c reductase= oxidises coenzyme Q and reduces cytochrome C

In complex IV, cytochrome C oxidase= oxidises cytochrome C, converts 2H+ AND 0.5 O2 into water.

28
Q

Steps involve in PKC activation

A

-PIP2 split into DAG and IP3 by enzyme phopholipase C
-IP3 binds to receptors in Endoplasmic R, causing calcium ions channels to open.
-The calcium ions then go out and binds to C2 domain of PKC. DAG binds to C1 domain, and PKC becomes activated.
-PKC binds to tumour supressor p53 to prevent tumour formation, to Ca v to open calcium ion channels and to IKK- alpha for B cell activation.

29
Q

How do NSAIDS work?

A

-Inhibit production of prostaglandins by inhibiting cyclooxygenase enzyme
-They inhibit blood clotting by inhibiting thromboxane.
-They relieve fever, pain and inflammation.

30
Q

Explain the action of ibuprofen.

A

Binds to COX inhibiting arachidonic acid from binding. It is a competitive inhibitor.

31
Q

Explain the action of aspirin.

A

-Irreversibly binds to COX-1 enzyme preventing arachidonic acid from binding. Inhibits production of thromboxane( can act as anticoagulant) and prostaglandins ( relieves pain).

-Effect can be reversed if more COX-1 enzyme synthesised.

32
Q

Pathogens routes of entry and examples

A

-Airway: Flu, meningitis
-GI tract: salmonella, typhoid fever, diarrhoea
-GU : syphilis
-External surface: Athlete’s foot
-Wounds and abrasions: anthrax and tetanus
-Insects bites: Yellow fever, malaria and lyme disease

33
Q

Explain the 3 phases if immune response

A

+Innate Immunity( 0-4 hours)
-Infection, recognition by non-specific effectors, removal of infectious agents.

+Early Induced response( 4-96 hours)
-Infection, recruit effector cells, recognition and activation of effector cells, removal of agent

+Adaptive Immune response( more than 96 hours)
-Infection, transport of antigen to lymphoid organs, recognition by B and T cells, clonal expansion, removal of agent.

34
Q

Name and explain barriers to infection

A

Mechanical- tight junction, movement of mucus by cilia, air and fluid flow across epithelium.

Chemical- defensins and cryptidins, gastric acid, fatty acids on skin and lysozymes on tears, sweat, saliva

Microbiological- formation of biofilms, flora in skin produce olicins and other antibacterial compounds.

35
Q

Name bactericidal agents from phagocytes

A

Acidification ph 3-4
-Secretion of toxic oxides: superoxides, H2O2 and hydroxyl radicals.
-Secretion of nitric oxide
-Secretion of enzymes like lysozymes.
-Secretion of defensins and cryptidins
-Secretions of competitors of bacteria like lactoferrin and vitamin B12-binding protein.

36
Q

Disease associated with neutrophils

A

-Alpha1 anti-trypsin deficiency: Excess tissue damage due to excess elastase being produced by neutrophils. Causes shortness of breath.

-Neutropenia: low neutrophil count due to chemotherapy or genetics.

-Chronic granulomatous disease: Neutrophils can’t do respiratory burst to kill pathogens.

37
Q

Disease associated with eosinophils

A

-Eosinophilia( high numbers of eosinophils): caused by parasites in GI, Hodgkin’s disease and Addison’s disease.
-Eosinopenia: Side effect of glucocorticoids use
-Eosinophilia-myalgia syndrome:

38
Q

What components are in the granules of basophils

A

-Histamines
-Proteoglycans
-Leukotrienes
-Cytokines
-Interleukin 4

39
Q

What is the response of a cell to being infected by a virus?

A

Release interferon alpha and beta which:
increase resistance to virus replication in surrounding cells, activate NK cells and stimulate antigen presentation.

40
Q

State the Law of mass action

A

Rate of a chemical reaction is proportional to the products of the concentration of the reactants.

41
Q

State the Receptor Theory

A

There is a systemathic relationship between concentraion of agonist drug and magnitude of response obtained.

42
Q

Name and describe drugs affecting noradrenaline release

A

Amphetamine- they enter cells via NET, reversing the pump direction and making it to pump NA out instead of in. It also displaces Na in VMAT, to be enclosed in vesicles instead of NA.

MOA inhibitors: Inhibit the degradation of NA into metabolites.

43
Q

Examples of places where thrombus develops due to endothelial injury.

A

Left ventricle at site of myocardial infarction
Ulcerated plaques of atherosclerosis
Injured endocardium
Inflammatory valve disease and prosthetic valves.

44
Q

Causes of endothelial injury

A

-Radiation injury
-Neoplastic involvement- formation of tumour
-Immunological injury
-Bacteria toxins
-Chemical agents

45
Q

Describe primary haemostasis

A

Process in which plug is formed after endothelial injury.
1. Platelet adhesion to endothelium via vWf and Glycoprotein Ib.
2. Platelet change shape
3. Platelet secrete granules containing, ADP, Thromboxane A2, vWf and Platelet factor 4 to recruit more platelets
4. Platelet recruitment
5. Platelet aggregation with Glycoprotein IIb and fibrinogen.

46
Q

Name 3 conditions related to platelet factors

A

-von Willebrand’s disease- deficiency of vW factors. Platelets can’t adhere to the endothelium.
-Bernard-Soulier Syndrome- deficiency of glycoprotein Ib, Platelets can’t bind to vWf to adhere to endothelium.
Glanzmann’s thrombosthenia- deficiency of glycoprotein IIb/IIIa complex, Platelets can’t do aggregation.

47
Q

Describe the antithrombic events

A

-Endothelial cells release tPA which stimulates activation of plasmin, enzyme in charge of fibrinolysis.

-Release of thrombomodulin which inhibits coagulation cascade

48
Q

What factors involved with blood flow aid in thrombosis and how

A

Turbulence and stasis. They both:
-Disrupt laminar flow.
- Prevent dilution of coagulation factors.
- Prevent coagulation inhibitors from reaching site of thrombosis.
-Promote endothelial cell activation

49
Q

Causes of primary hypercoagulability-

A
  • Antithrombin III deficiency’
    -Factor V Leiden mutation
  • Protein C and S deficiency
50
Q

Causes of secondary hypercoagulability

A

High risk: MI, DIC, bed rest, cardiac arrest, tissue damage

Low risk: cardiomyopathy, nephrotic syndrome, atrial fibrillation, sickle cell anaemia and smoking.

51
Q

Symptoms of arterial thrombosis

A

-Loss of pulse distal to thrombosis
-Painful, Pale, Perishing cold, Paraesthesia and pulseless.
-Necrosis and gangrene of that area that may even result to autoamputation.

52
Q

Symptoms of venous thrombosis

A

-Superficial veins: tenderness, swelling, pain, congestion
-Deep veins: Positive Hoffman’s sign( pain in deep calf during dorsiflexion) and oedema in ankle and foot.

53
Q

Source of emboli

A

-Thrombus(99% of cases)
- Fat droplets
- foreign bodies
-bubbles of gas
- bone/bone marrow fractures
-atheroma debris
- tumour

54
Q

Fat Embolism Syndrome causes

A

Mechanical injury due to microaggregates of fat.
Chemical injury due to free fatty acids causing toxic injury in endothelium of blood vessels.

54
Q

Fat Embolism Syndrome causes

A

-Mechanical injury due to microaggregates of fat.

-Chemical injury due to free fatty acids causing toxic injury in endothelium of blood vessels.

55
Q

Fat Embolism Syndrome consequences

A

-Pulmonary insufficiency: tachypnoea, dyspnoea and tachycardia.
-Anaemia
-Thrombocytopenia
-Neurologic symptoms: irritability, delirium, restlessness and coma

56
Q

Causes of infarction

A

-Traumatic rupture
-Vasospasm
-compression of vessel
-twisting of vessel
-atheroma expansion

57
Q

Factors influencing infarction

A

-Tissue sensitivity to hypoxia
- Concentration of oxygen in blood: anaemic and cyanotic patient have higher risk.
- Rate of development of occlusion.
-Whether tissue/organ has dual or single blood supply.

58
Q

Types of infarction

A

RED- haemorrhagic- caused by venous occlusion in loose tissues like lungs or valves.
WHITE- anaemic. Caused y arterial occlusion in solid organs
SEPTIC/BLAND- bacteria creates colonies inside blood vessels and occlude them.

59
Q

Coagulation inhibitors

A

+Protein C- activated by thrombomodulin.
+ Cofactor-factor S, degrades factors VIIIa and Va.
+ Antithrombin, inhibits factors IIa and Xa.
+Heparin cofactor II- inhibits factor IIa

MD2002 (10 decks)

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