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MRCS A - Physiology + Pathology > Physiology > Flashcards

Physiology Flashcards

1
Q

Two mechanisms by which a metabolic acidosis will occur?

A

Gain of a strong acid

Loss of a base

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2
Q

How do you figure out anion gap, what is normal?

A

(Na + K) - (Cl + HCO3)

should be between 10 and 18

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3
Q

Metabolic acidosis - normal anion gap vs raised anion gap causes?

A 
Normal anion gap = hyperchloraemic metabolic acidosis
GI loss e.g. vomiting
RTA
Drugs e.g. acetazolamide
Addisons

Raised anion gap:
Lactate - Type A = perfusion e.g. shock, hypoxia, burns.
- Type B = Metabolic e.g. metformin toxicity
Urate raised in renal failure
Acid poisoning e.g. salicylates or methanol

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4
Q

Causes of metabolic alkalosis?

A 
Vomiting
Diuretics
Hypokalaemia 
Primary hyperaldosteronism 
Cushings 
Barters Syndrome = same as loop diuretics
Gittlemans syndrome = same as thiazides 
CAH
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5
Q

Mechanism of metabolic alkalosis?

A

Activation of RAAS system is key
Aldosterone causes reabsorption of Na in exchange for H in the DCT
So if ECF depleted = lose Na = more aldosterone = lose H

If hypokalaemia, K shifts extracellular. This means H shifts intracellular to maintain neutrality

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6
Q

Respiratory acidosis cause and examples?

A

rise in carbon dioxide due to alveolar hypoventilation
Often get metabolic compensation

COPD
Decompensated asthma / CCF
Sedative drugs e.g. benzo’s and opiates

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7
Q

Respiratory alkalosis - mechanism and causes?

A

Hyperventilation leading to low carbon dioxide

Psychogenic e.g. anxiety
Hypoxia causing subsequent hyperventilation
Early salicylate poisoning
CNS stimulation e.g. strokes, SAH and encephalitis

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8
Q

Vascular changes In acute inflammation?

A

Inflammatory cells exit at site of injury > disrupts starlings forces > protein rich exudate as cell walls become more permeable

High fibrinogen content may lead to clots

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9
Q

In acute inflammation what are the vasodilators vs vasoconstrictors?

A

Vasodilators = PGE, histamine, NO, complement C5a and lysosomal compounds

Vasoconstrictor = serotonin. (although in normal tissue it vasodilators)

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10
Q

Sequelae of acute tissue injury?

A

Resolution = stimulus removed and normal architecture returned

Organisation = delayed removal of exudate, tissue undergoes organisational change and usually fibrosis

Suppuration = forms empyema or abscess > large quantities of dead neutrophils sequester

Chronic inflammation = coupled inflammatory and reparative acts, usually when initial infection poorly managed

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11
Q

What is the histological hallmark of acute inflammation?

A

Neutrophil polymorphs

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12
Q

Acute vs chronic inflammation?

A

Acute is usually to existing vasculature, chronic angiogenesis dominates

Acute = neutrophils, chronic = macrophages, plasma cells and lymphocytes

Chronic only heals by fibrosis, acute has the 4 sequelae

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13
Q

What is the cell type of granuloma?

A

Aggregation of macrophages, with epithelial like arrangement

Large giant cells may be found at the periphery

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14
Q

Mediators of chronic inflammation?

A

GF’s released by macrophages e.g. IFN and fibroblast GF

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15
Q

Mechanism of necrosis?

A

Loss of tissue perfusion = hypoxia and cannot generate ATP
Cell membrane integrity lost, lose ATP dependant. transporters

Influx of water, ionic instability + cellular lysis

Release of intracellular contents = inflammatory response

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16
Q

Mechanism of apoptosis?

A

Programmed cell death
Energy dependent pathways activated by intracellular pathways
Activation of caspases via BCL2 and FAS ligand binding
You get:
- DNA fragments
- Mitochondrial function ceases
- Nuclear and cellular shrinkage

Phagocytosis of cell DOES NOT OCCUR, develop apoptotic bodies

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17
Q

Coagulative necrosis?

A

Seen in most organs
Tissue initially firm, soft once digested by macrophages
In later stages > cellular outlines seen, with loss of intracellular detail

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18
Q

Colliquative necrosis?

A

Occurs in tissue with no supporting stroma
Dominant pattern in CNS
Necrotic site eventually becomes encysted

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19
Q

Caseous necrosis?

A

No definable structure
Amorpheous eosinophilic tissue
Classic in TB

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20
Q

Gangrenous necrosis?

A

Necrosis with putrefaction of tissue
May complicate ischaemia
Hb degenerates and results in iron sulphide deposition = black tissue

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21
Q

Fibrinoid necrosis?

A

Seen on arterioles of patients with malignant HTN

Necrosis of smooth muscle walls > plasma may extravasate into media with fibrin

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22
Q

4 phases of wound healing, time frame and cells present at each?

A
  1. Haemostasis = seconds to minutes
    - vasospasm of vessels and platelet plug formation = generation of fibrin clot
    - CELLs = erythrocytes and platelets
  2. Inflammation = days
    - Neutrophils migrate = GF’s e.g. VEGF
    - fibroblasts replicate
    - Macrophages and fibroblasts = matriculates regeneration
    - CELLS = macrophages, fibroblasts and neutrophils
  3. Regeneration = weeks
    - Platelet derived GF’s
    - Fibroblasts form collagen network
    - Angiogenesis
    - granulation tissue
    CELLS = fibroblasts, endothelial cells and macrophages
  4. Remodelling = weeks to year
    - Fibroblasts differentiate > myofibroblasts = wound contraction
    - micro vessels regress = pale scar
    CELLS = myofibroblasts
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23
Q

Scar problems - hypertrophy vs keloid?

A

Hypertrophy:
Excessive collagen
Nodules = randomly arranged within, parallel on surface
Confined to extent of original wound

Keloid:
Extends beyond original wound
No nodules
Does not regress over time

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24
Q

Drugs impairing wound synthesis?

A

NSAIDS
Steroids
Anti-cancer drugs
Immunosupressive’s

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25
Q

Secondary closure vs delayed primary?

A

Delayed primary is waiting a few days after surgery, but before granulation tissue macroscopically visible

Secondary = spontaneous or post-surgery once granulation tissue formed

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26
Q

What is cerebral perfusion pressure?

A

MAP - intracranial

> 70 is acceptable

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27
Q

MAP equation?

A

Diastolic + 0.33(systolic - diastolic)

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28
Q

4 types of opioid receptors, where they are found and effect?

A

Delta = CNS = analgesic an anti-depressant

Kappa = CNS = analgesic + dissociative

Mu. = central and peripheral = analgesia, miosis, decreases gut motility

Nociception receptor = CNS. = appetite and tolerance to Mu receptors

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29
Q

Pain - A fibres vs C fibres?

A

A =. high intensity mechanical stimulation

C = high intensity mechanothermal stimulation

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30
Q

Neuropraxia vs axonotmesis vs neurotmesis?

A

Neuropraxia =. nerve intact, electrical conduction affected

Axonotmesis = axon damaged, myelin sheath preserved
Wallerian degeneration

Neurotmesis=. disruption of axon, sheath. and surrounding connective tissue
Wallerian degeneration

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31
Q

Process of wallerian degeneration?

A

Axonal damage
Myelin sheath degrades and macrophages and Schwann cells infiltrate and clear debris
Schwann cells extrude their own axonal sheath, aligning to form bungner bands and express surface molecules guiding regeneration

Near complete recovery PNS, minimal in CNS (uses oligodendrocytes)

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32
Q

Does intrinsic pathway have major or minor role in clotting, how does it start and which blood test is it?

A

Minor role

Formation of primary complex on collagen with high molecular weight kininogen + F12

APTT

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33
Q

WEPT?

A

Extrinsic pathway = main pathway.
- needs tissue factor to be released from damaged tissue = binds to factor 7.

PT

Warfarin = 2, 7, 9, 10

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34
Q

What is the common pathway in clotting?

A

Factor X to Xa
Xa then with the help of 5a converts prothrombin to thrombin
Thrombin the converts fibrinogen to fibrin = clot

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35
Q

How does clot respiration happen?

A

Plasminogen converted to plasmin

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36
Q

What factors does heparin affect vs warfarin?

What does lover disease affect?

A

Warfarin = 2, 7, 9, 10

Heparin = 2, 9, 10, 11

Liver = all except factor 8 as this is made in endothelial cells of the liver = less susceptible to damage

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37
Q

Interpretation of abnormal clotting:

  1. abnormally raised everything
  2. raised APTT, bleeding and PT normal
  3. Raised APTT and bleeding time, PT normal
  4. Raised APTT and PT, bleeding time Okay
  5. only raised PT
A
  1. DIC
  2. Haemophilia
  3. vWD
  4. Heparin therapy or vitamin k deficiency
  5. Warfarin
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38
Q

What is the most common inherited bleeding disorder?

A

vWD

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39
Q

What is vW factors role?

A

Promotes platelet adhesion to damaged endothelium

Also involved in transport and stabilisation of factor 8

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40
Q

Mx of vWD?

A

Tranexamic acid for minor procedures

If more severe bleeding can be DDAVP

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41
Q

Stored RBC has lower levels of what?

What is the effect of this?

A

Lower levels of 2,3-DPG

Means higher affinity to oxygen, so less likely to give it up to metabolising cells

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42
Q

What deficiencies are you at risk of during RBC transfusion?

A

Factor 5 and 8

As well as thrombocytopaenia

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43
Q

Commonest adverse reaction in RBC transfusion?

A

Pyrexia

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44
Q

Which blood products can be. ABO. incompatible?

A

Platelet concentrate and FFP

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45
Q

What is FFP?

Most common adverse reaction of FFP?

A

Clotting factors, albumin and immunoglobulin

Urticaria

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46
Q

What is in cryoprecipitate?

A

Factor 8 and fibrinogen

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47
Q

Transfusion reactions:
Immediate
Urticaria, rash + angioedema

A

Allergic reaction

Recipient IgA deficiency > anti-IgA IgE

Mx = slow transfusion and chlorphenamine

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48
Q

Transfusion reactions:
<6 hours, SOB, cough, raised JVP and leg swelling
Known HF

A

CCF

slow transfusion, oxygen and furosemide

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49
Q

Transfusion reactions:
<6 hours
SOB + cough, CXR bilateral pleural infiltrates
Pneumonia on admission

A

TRALI = ARDS
Anti WBC antibodies in donor PLASMA

Mx = stop transfusion and manage ARDS

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50
Q

Transfusion reactions:
Within minutes the patient is agitated, pyrexial and in shock
Massive AKI

A

Haemolytic reaction

ABO incompatibility
Also get DIC

Mx = stop and treat DIC

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51
Q

Transfusion reactions:
12 hours
Fevers, rigors and shock following platelets

A

Bacterial contamination
Most commonly seen with platelets

Mx = stop transfusion, Tax and gent

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52
Q

Transfusion reactions:

12 hours after, fever and rigors

A

non-haemolytic febrile reaction

Recipient anti-HLA antibodies

Mx = slow transfusion + paracetamol

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53
Q

Transfusion reactions:

1 week later, jaundiced anaemic and blood in urine

A

Delayed haemolytic
Due to recipient anti-Rh antibodies

Extravascular haemolysis

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54
Q

Transfusion reactions:

1 week after transfusion, purpura all over body and low platelets

A

post-transfusion purpura

Allogenic anti-bodies attack recipient and donor platelets

Mx = IVIG and platelet transfusion

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55
Q

Transfusion reactions:

2 weeks later, diarrhoea rash and jaundiced

A

GVHD

Due to viable lymphocytes, given in the blood to an immunocompromised patient

Mx = irradiated blood should be given, Mx after is steroid based

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56
Q

Non-immune transfusion reactions?

A

Low calcium, hyperkalaemia
CCF
infections

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57
Q

How does warfarin work?
Factors it affects?
Things that potentate warfarin?

A

Inhibits reduction of vitamin K to its active hydroquinone form

2, 7, 9, 10

Liver disease, CYP450 inhibitors e.g. amiodarone and ciprofloxacin, cranberry juice, NSAIDs

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58
Q

Warfarin SE’s?

A

Haemorrhage
Teratogenic
Skin necrosis

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59
Q

Management of high INR on warfarin?

A

Major bleeding / urgent reversal for surgery:
Stop warfarin
IV vitamin K
Prothrombin complex (bereplex 50u/kg)
- if no prothrombin complex then cryoprecipitate

INR > 5 with any bleeding:
Stop warfarin
IV vitamin K 3-5mg
Recheck in 6 hours and repeat if still high
Start warfarin when INR <5
INR >8 no bleeding:
Stop warfarin 
Oral vitamin K
Check ± repeat
Restart when INR <5

INR 5-8 no bleeding:
Hold 1-2 doses
reduce subsequent dosing

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60
Q

Heparin:
Mechanism?
why its better than unfractionated?
complications?

A

Causes formation of complexes between anti-thrombin and activated thrombin

Longer half life, lower risk of HIT, little effect on APTT

Bleeding, osteoporosis, HIT (2 weeks after dosing)

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61
Q

How does tranexamic acid work?

A

Inhibits conversion of plasminogen to plasmin = plasmin degrades clots

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62
Q

Causes of severe thrombocytopenia?

A

ITP
DIC
TTP
Haematological malignancy

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63
Q

Causes of moderate thrombocytopenia?

A 
Liver disease and alcohol 
Hypersplenism 
Viral infection  
HIIT
Pregnancy 
B12 deficiency
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64
Q

Mechanism of DIC?

A

Dysregulation of coagulation and fibrinolysis
Tissue factor gets exposed to general circulation (doesn’t normally happen)
This causes clotting cascade ++
This then uses up all the clotting factors (namely 5 and 8) = bleeding ++

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65
Q

Clinical features of DIC and causes?

A

bleeding
Cough and SOB and fever

All bleeding parameters raised

Causes = sepsis, malignancy, trauma and liver disease

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66
Q

Antibodies for anti-phospholipid syndrome?

A

Anti-cardiolipin

Lupus anticoagulant

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67
Q

Criteria for anti-phospholipid syndrome?

A

Thrombus in any organ, or pregnancy event (1 miscarriage >10 weeks, 3 <10 weeks, or premature <34 weeks due to eclampsia)

Plus persistently +ve antibody titres

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68
Q

Clinical features of anti-phospholipid and Mx?

A

Thrombus / pregnancy event
Livedo reticularis
Cardiac valve lesions
Thrombocytopaenia

Mx = heparin initially then warfarin

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69
Q

Warm AIHA - mechanism, causes, Ix and Mx?

A

IgG mediated at 37 degrees
Causes = SLE, RA, Evans and idiopathic

Ix = extravascular haemolysis, spherocytes and DAT+ve

Mx = steroids, immunosuppression and splenectomy

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70
Q

Cold AIHA - mechanism, causes, Ix and Mx?

A

IgM at 4-degrees

Causes = idiopathic, neoplasm and mycoplasma

Intravascular haemolysis, acrocyanosis and raynauds, DAT+ve for complement only

Mx = avoid cold and rituximab

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71
Q

What diseases and Ab’s associated with paroxysmal cold haemoglobinuria?

A

Measles, chickenpox and mumps

IgG Donath-Landsteiner Ab’s bind RBC’s in the cold, then haemolyse when rewarmed

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72
Q

PNH - mechanism?

A

Due to an acquired deficiency in glycoprotein-phosphatidylinositol = cell membrane more sensitive to complement

Also have lack of CD59 on platelet cell membranes = predisposes to aggregation = clotting

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73
Q

PNH - clinical features, Ix and Mx?

A 
Pancytopaenia
Haemoglobinuria 
Thrombosis = budd chiari syndrome
Haemolytic anaemia
Rarely can progress to aplastic anaemia

Ix:
Blood = pancytopaenic
Flow cytometry = low CD59 and CD55

Mx = blood product replacement, anti-coagulation and monoclonal antibody eculizumab

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74
Q

HUS - mechanism and causes?

A

Due to endothelial damage leading to microvascular thrombosis

90% occurs in children due to E.Coli 0157:H7
Pregnancy
Tumours
Drugs = ciclosporin and COCP

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75
Q

HUS - Clinical features, Ix and Mx?

A

Triad = acute renal failure, MAHA and thrombocytopaenia
+ bloody diarrhoea and abdominal pain

Ix = FBC will show anaemia and thrombocytopaenia. U+E’s plus stool culture

Mx:
Supportive = fluids, blood products and dialysis
No role for antibiotics
Plasma exchange in severe ones with no diarrhoea

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76
Q

TTP - mechanism?

A

Genetic or acquired defect in von Willebrand cleaving enzyme ADAMTS13

= large von willebrand multimers = platelet aggregation

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77
Q

TTP - clinical features, Ix and Mx?

A 
Pentad:
Fever
MAHA
Acute renal failure
Thrombocytopaenia
CNS signs - confusion and seizures

Ix = same as HUS = anaemia, thrombocytopaenia and fragmented blood film. U+E’s

Mx = plasmapheresis

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78
Q

What is the commonest inherited haemolytic anaemia in Northern Europe?
Inheritance pattern?

A

Hereditary spherocytosis

Autosomal dominant

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79
Q

Hereditary spherocytosis - Clinical features, diagnosis and Mx?

A

FTT, jaundice and pigment stones = colic
Splenomegaly
Aplastic crisis precipitated by parvovirus B12

Dx = osmotic fragility test.
- also spherocytes on the film and DAT-ve

Mx:
No splenectomy until age 6
Pre splenectomy vaccine course
After = BenPen and annual influenza + 5-yearly pneumococcal

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80
Q

Hereditary spherocytosis - mechanism ?

A

Defect in structural membrane proteins = abnormal cells = removed by spleen

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81
Q

G6PD deficiency - inheritance, mechanism and triggers?

A

Male X-linked disorder
Defect in pentose phosphate shunt = reduced NADPH production = RBC oxidative damage

Triggers for haemolysis:
Broad beans / lava beans, moth balls
Infection
Drugs = anti-malarial, ciprofloxacin and sulphonamides

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82
Q

G6PD deficiency - clinical features, investigations and management?

A

Neonatal jaundice, intravascular haemolysis, gallstones

Ix = film = irregularly contracted cells, bite cells, Heinz bodies

Mx = Treat cause / avoid precipitant
Transfusion

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83
Q

Pyruvate kinase deficiency - inheritance and mechanism?

A

Autosomal recessive

Defect in ATP synthesis = rigid red cells = removed in spleen

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84
Q

Pyruvate kinase deficiency = clinical features, Ix and Mx?

A

Jaundice, anaemia and splenomegaly (JAS)

Ix = PK assay, blood film > Burr cells and echinocytes

Mx often not needed. Can transfuse and splenectomy

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85
Q

Mechanism behind polycythaemia vera?

A

95% mutation in Jak2

Clonal proliferation of marrow stem cell = increased RBC. volume

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86
Q

Clinical features of polycythaemia vera ?

A

Hyperviscocity = headaches, visual disturbance and thrombosis
Pruritus after hot baths = histamine release
Splenomegaly and hepatomegaly
Haemorrhage
HTN

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87
Q

Mx of polycythaemia vera?

A

Aspirin, venesection

If high thrombosis risk = hydroxycarbamide = cytoreductive

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88
Q

Causes of secondary polycythaemia?

A

Hypoxia = COPD, altitude, smoking

EPO = renal cysts

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89
Q

Mechanism of essential thrombocytopaenia?

A

Sustained dysregulated production of megakaryocytic from bone marrow = increasing circulating numbers of platelets

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90
Q

Clinical features of essential thrombocytopaenia?

A 
50% asymptomatic 
Thrombosis
Bleeding
Splenomegaly 
Burning pain in extremities on heat = erythromelalgia
Livedo reticularis
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91
Q

Management of essential thrombocytopaenia?

A

Conservative = stop smoking, diet, exercise
Plateletpheresis

Medical - anti platelet e.g. aspirin

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92
Q

Mechanism behind primary myelofibrosis?

A

increased clonal proliferation of haematopoietic cells in bone marrow, particularly megakaryocytic.
These abnormal cells produce excess growth factor = excess fibroblasts = collagen deposition and fibrosis

This means fibrosis in bone marrow, cannot make cells there so become pancytopaenic

Also means extra medullary haematopoiesis = hepatomegaly and splenomegaly

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93
Q

Clinical features and investigations of primary myelofibrosis?

A

Old person, massive splenomegaly
Pancytopaenic = anaemia, infections and bleeding

Blood film = tear drop poikilocytes
Unobtainable BM aspirate, dry tap. Means need trephine biopsy

High rate and LDH

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94
Q

Prognosis of primary myelofibrosis?

A

Median 5-year survival

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95
Q

Management of primary myelofibrosis?

A

Asymptomatic = folic acid and pyridoxine, peginterferon alpha

Symptomatic = BM transplant, not if >65

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96
Q

Mechanism of sickle cell?

A

Abnormal synthesis of HbS

Glutamate substituted for non-polar valine = fragile and haemolyse

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97
Q

Clinical features of sickle cell anaemia?

A

SICKLED

Splenomegaly
Infarct = stroke, spleen, retinal floaters
Crises = pain
Kidney failure
Liver and. lung disease = SOB, jaundice, cough
Erection issues
Dactylitis

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98
Q

Crisis type in sickle cell?

A

Thrombotic = pain, could be any organ really

Sequestered = pooling of blood due to sickling in organs e.g. spleen or lungs

Aplastic crisis - due to parvovirus

Haemolytic crisis (rare)

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99
Q

Management of sickle cell?

A

Crisis = analgesia, hydrate, warm and oxygen
Antibiotics if infection
Exchange transfusion

Long term = Penicillin and immunisations, folate, hydroxycarbamide if multiple crises

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100
Q

Surgical complications of sickle cell?

A

Acute cholecystitis
Avascular necrosis
Bowel ischaemia

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101
Q

Mechanism of ALL?

A

Arrest of maturation of lymphoblasts and excessive production of immature lymphoblasts = no space for the other cells to form

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102
Q

Clinical features of ALL?

Common age of onset?

A

3-5 years

Pancytopenia = infection, bruising and anaemic
Bone pain
Splenomegaly and hepatomegaly due to extra medullary haematopoiesis
Testicular swelling

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103
Q

Investigations of ALL?

A

BM aspirate > 20% blasts
WCC raised, RBC/platelet/PMN low

XR / CT may show mediastinal LN’s

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104
Q

Management of ALL?

A

Supportive = fluids and allopurinol
- prophylactic antibiotic and permanent line for chemo
Induction chemo, consolidation and maintenance
Longer chemo in boys due to testes

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105
Q

Mechanism of AML?

A

Arrest of differentiation of the myeloblast at a point in it differentiation.
Can occur at any of multiple stages
Causes abnormal blast cells in peripheral blood and BM

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106
Q

Clinical features of AML?

Who it tends to affect?

A

Pancytopenia
Infiltration = hepatosplenomegaly, gum hypertrophy and bone pain
Increased WCC = hyperviscocity

adults

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107
Q

Ix and management of AML?

A

WCC high, RBC + platelets low
Film = peripheral blasts
BM aspirate > 20% blasts, Auer rods under MPO stain

Mx = supportive + chemo ± BMT/SCT

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108
Q

Commonest leukaemia in western world?

A

CLL

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109
Q

who does CLL affect?

A

Elderly males

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110
Q

Mechanism of CLL?

A

Monoclonal proliferation of mature lymphocytes - usually B-cells

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111
Q

Clinical features of CLL?

A

Often asymptomatic
Constitutional
Bleeding + infections
Infiltrates = splenomegaly + LN’s ++

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112
Q

Ix of CLL?

What would make it small lymphocytic leukaemia?

A

B lymphocytes > 5 x10^9
Clear cells
DAT+ve

SLL = B cells mainly in spleen, <5x10^9

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113
Q

What is Binet staging for, and the staging please maestro?

A

CLL

A <3 lymphoid areas = 12 year prognosis
B > 3 lymphoid ares = 5-year survival
C Hb or platelets <100 = 2 year survival

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114
Q

Management of CLL?

A

Supportive if Binet A+B

Chemo if Binet C

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115
Q

Mechanism of CML?

A

Myeloid hyperplasia

Due to philadelphia chromosome = t(9:22) translocation = BCR-ABL gene

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116
Q

Age of presentation for CML?

Clinical features?

A

60

Anaemia, bruising and bleeding
MASSIVE splenomegaly and hepatomegaly
Constitutive symptoms

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117
Q

Phases of CML?

A

chronic =. 80% progress to accelerated phase
Over production of mature neutrophils, basophils and myelocytes

Accelerated = 10-19% blasts

Blast phase = > 20% blasts. Basically AML

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118
Q

Ix and Mx of CML?

A

Raised WBC’s
Low Hb and platelets if in blast/accelerated phase
Raised urate levels
Phil+ve

Imatinib

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119
Q

Mechanism of NHL?

A

Lymphoma begins in lymphocytes = growth and expansion of monoclonal population of malignant lymphocytes

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120
Q

Risk factors for lymphoma?

A

Constant antigen stimulation:

  • H. Pylori = MALT
  • Coeliacs = Small bowel T-cell lymphoma
  • Hashimotos
  • Sjogrens

Infection:
HTLV1 infects T cells
EBV infects B cells
Hep C

HIV

Iatrogenic = immunosuppression following solid organ transplantation

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121
Q

NHL clinical features?

NHL Ix?

A

75% present with painless LN’s. Multiple sites and symmetrical
Splenomegaly
B-symptoms

Pancytopaenia
Hyperviscocity
LN and BM biopsy for classification
Staging with MRI/CT

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122
Q

Classification of NHL?

A

B-cell:
Aggressive:
diffuse large B cell
Burkitts

Indolent:
MALT
Follicular

T-Cell associated:
Adult T cell lymphoma
Enteropathy associated

123
Q

Mx of NHL?

A

R-CAVP

Rituximab, cyclophosphamide, adriamycin, vincristine, prednisolone

124
Q

Classic Burkitt’s NHL signs?

A

C-myc gene

Starry sky

125
Q

Hodgkins lymphoma - bimodal distribution? Mechanism?

A

20-29 and >60

Lymphoma arising from mature B-Cells, but has reed Sternberg cells

126
Q

Under the microscope what cells distinguish NHL vs HL?

Which has. better prognosis?

A

HL has reed-sternberg cells

HL has better prognosis

127
Q

Types of HL and best vs worst prognosis?>

A

Nodular sclerosing = most common, 70%

Mixed cellularity = 20%, best prognosis

Lymphocyte predominant = 5%, BEST PROGNOSIS

Lymphocyte depleted = rare, worst prognosis

128
Q

Clinical features of HL and staging?

A 
LN's, painlessly, mainly cervical 
- in questions more pain on alcohol 
B-symptoms
Pel-ebstein fever
Hepato/splenomegaly
Ann-Arbour staging
1 = single LN region
2 = > 2 regions, same side of diaphragm
3 = >2 either side of diaphragm
4 = Spread beyond nodes
129
Q

Ix for HL?

Mx?

A

LN excision > must be COMPLETE LN = reed sternberg cells
CT-CAP for staging

Chemo ABVD:
Adriamycin, bleomycin, vinblastine, DTIC
4-weekly cycles x6, preserves fertility
SE’s = pulmonary fibrosis and cardiomyopathy

130
Q

Multiple myeloma mechanism?

A

Clonal proliferation of plasma cells = monoclonal IgG or IgA raised
Clones may produce free light chains
These can. be excreted via kidneys = Bence-Jones proteins in urine

Clone produce IL-6, inhibits osteoblasts and activates osteoclasts

131
Q

Clinical features of multiple myeloma?

A

CRAB
Calcium raised
Renal impairment - acute tubular necrosis due to free light chains causing inflammation
Anaemia
Bone lesions = #’s and can get spinal cord compression

132
Q

Ix for multiple myeloma?

A

Electrophoresis = monoclonal Ig
Urine = raised specific gravity
BM aspirate
X-ray = punched out lytic lesions

133
Q

characteristics of Waldenstroms?

A

IgM only
Older men
Systemic upset, hyperviscocity + hepatosplenomegaly + LN’s

134
Q

Mechanism of amyloidosis?

A

Extracellular deposition of an insoluble fibrillary protein = amyloid
Leads to organ dysfunction

135
Q

Cause of AL amyloid vs AA?

A 
AL = derived from plasma cells producing amyloidogenic light chain
Primary = Occult plasma cell proliferation
Secondary = Myeloma, MGUS, Waldenstroms

AA = from serum amyloid in chronic inflammation
RA, IBD, chronic infection

136
Q

Clinical features of AA vs AL amyloidosis?

A 
AL:
Renal - nephrotic syndrome
Heart - restrictive cardiomyopathy 
Nerve - Carpal tunnel, neuropathy
GIT - Malabsorption, perforation
Vascular - Periorbital purpura

AA:
Renal
Hepatosplenomegaly

137
Q

Ix and Mx of amyloidosis?

A

Congo red stain = apple green birefringence
Serum amyloid precursor scan
SURGIAL BIOPSY OF RECTUM

Mx:
AL = treat myeloma
AA = Treat underlying cause

138
Q

4 acute porphyrias?

Enzyme deficient in each?

A

Plumboporphyria, acute intermittent porphyria, hereditary coproporphyria, variegate porphyria

Plumboporphyria = ALA dehydratase /. PGB synthase
AIP = HMB synthase
Hereditary = coproporphyrinogen oxidase
Variegate porphyria = protoporphyrinogen oxidase

139
Q

features of plumboporphyria?

A

PGB synthase
90% abdominal pain
Motor neuropathy
ONLY ONE WITH LOW PBG

140
Q

Features of AIP?

A

HMB synthase

High ALA and. PBG

Abdominal pain, red urine on standing, motor neuropathy, HTN and tachycardia

141
Q

Ix and Mx of AIP?

A

Deep red urine on standing with raised urinary porphobilinogen (PBG)
Raised serum levels of ALA and PBG

Mx = analgesia, fluids and IV haematin

142
Q

Features of hereditary coproporphyria?

A

Coproporphyrinogen oxidase

coproporphyrinogen in stool
Neurovisceral symptoms as build up of coproporphyrinogen = HMB synthase inhibitors = ALA build up

Photosensitive skin, blistering and pigment change

143
Q

Features of variegate porphyria?

A

Protoporphyrinogen oxidase
Build up of protoporphyrinogen in stool

Neurovisceral as it inhibits HMBS = ALA build up

Photosensitive skin, blistering and pigment changes

144
Q

Non acute porphyria?

A

Porphyria cutanea tarda = uro. decarboxylase

145
Q

Porphyria cutanea tarda - features, investigations and. Mx?

A

photosensitive rash, blistering, skin fragility
Hyperpigmentation

Classically occurs delayed post sun exposure

Urine = elevated uroporphyrinogen and pink colour under woods lamp

Mx = avoid sun, iron chelators + chloroquinine

146
Q

Features of lead poisoning, what blood level is signifiant for diagnosis + management?

A

Abdo pain, peripheral neuropathy, constipation, blue lines on gum margin in 20%

> 10mcg/dl is signifiant

Mx = DMSA, penicillamine, EDTA

147
Q

Indications for a splenectomy?

A 
Trauma - hilar injury
ITP
AIHA
Rupture e.g. EBV
Hereditary spherocytosis 
Splenic vein thrombosis (diagnosed with CT angio)
148
Q

Complications of splenectomy ?

A 
Haemorrhage
Pancreatic fistula
Gastric ileus
lower lobe left atelectasis 
Susceptibility to encapsulated organisms - strep pneumo, HI, meningococci
149
Q

Outline of procedure for emergency splenectomy e.g. trauma?

A

Midline incision under GA
Pack all four quadrants
Remove packing and assess damage
If hilar injury or severe parenchymal injury = remove

divide the short gastric vessels and ligate
Clamp splenic artery and vein - double clamp on patient side as safety precaution
When done wash out abdomen, place drain

Some surgeons implant portion of spleen into the omentum

150
Q

In splenectomy where do the short gastric arteries lie?

Why might you find amylase in your drain post-splenectomy?

When should you administer platelet transfusion in ITP splenectomy?

A

Within the gastrosplenic ligament

Damage to pancreatic tail

After clamping of splenic artery

151
Q

Immunisations for splenectomy?

A

pneumovax, HiB, Men C and flu two weeks before surgery

Then yearly flu and 5-year pneumococcal

Penicillin V

152
Q

Blood film signs of splenectomy?

A

Target cells
Howell Jolly bodies
Pappenheimer
Acanthocytes

153
Q

Oncovirsues - EBV, HPV 16/18, HPV8, Hep, HTLV-1?

A

EBV = Burkitts, Hodgkins lymphoma, post-transplant lymphoma + nasopharyngeal carcinoma

HPV 16/18 = cervical anal penile and vulval cancer

HPV8 = Kaposi’s

HTLV-1 = Adult T-ell leukaemia

Hep B/C = hepatocellular carcinoma

154
Q

Via vagus to the heart what do the parasympathetic fibres release?
What do the sympathetic fibres release?

A

Parasymp. = ACh

Symp. = noradrenaline. Noradrenaline binds to B1 receptors on SA node and increased depolarisation rate

155
Q

4 phases of a myocardial action potential?

A

Phase 0 = rapid depolarisation > sodium influx

Phase 1 = early depolarisation > Potassium efflux

Phase 2 = plateau > Slow calcium influx

Phase 3 = final depolarisation > Potassium efflux

Phase 4 = restoration > Na/K/ATPase pump causes slow influx of potassium until threshold potential reached

156
Q

Cardiac cycle - mid and late diastole, early and late systole?

A

Mid diastole = basically passive ventricular filling
AV valves are open, outflow valves shut. Ventricles hold 80% of final volume.
Aortic pressure is high.

Late diastole = active ventricular filling
Atria contract, ventricles get last 20% volume

Early systole = ventricular contraction
AV valves shut, ventricular pressure rises, contraction
AV valve bulges back into the atria = C-wave on JVP
Blood is ejected as pressures exceed aortic and pulmonary pressures
Atrial pressure will decrease as ventricles shorten and contract pulling them down = x-descent on JVP waveform

Late systole = ventricles relax
Pressure drops, brief period of retrograde flow then aortic valve closes
Atrial pressure begin to exceed ventricular > AV valve opens > passive filling begins
Atrial pressure falls here = Y-descent on JVP

157
Q

Laplaces law?

A

For hollow organs, with circular cross section, total circumferential wall tension = pressure x radius /2

Total luminal pressure = radius x transmural pressure

158
Q

Starlings law?

A

Increased in end diastole volume = larger stroke volume

Up to a point but stretch the cardiac tissue too much and then starts to decrease again

159
Q

Where are baroreceptors located, what are their nerves they travel in and what stimulates them?

A

Aortic arch and carotid sinus

Aortic arch = via vagus
carotid sinus = glossopharyngeal

Stimulated by aortic stretch

160
Q

What happens when baroreceptors are stimulated by aortic stretch?

A

Increased parasympathetic to SA node

Decreased sympathetic too…
Ventricular muscle = decreased contractility
Venous system = increased compliance
Decreased peripheral arterial vascular resistance

161
Q

Where are atrial stretch receptors located?

A

In atria between junction of pulmonary veins and vena cava

Low pressure sensors

162
Q

What happens when the atrial stretch receptors are stimulated?

A

Increased stretch = increased parasympathetic activity + release of ANP
If rapid filling causes increased HR = Bainbridge reflex

Decreased stretch = increased sympathetic activity = decreased renal blood flow, activates RAS system = sodium and water retention

163
Q

JVP waveform - What is absent in AF?
What does this wave usually signify?
When might this wave be large?

A

a waves

Atrial contraction

Any cause of RVH e.g. pulmonary stenosis/HTN, tricuspid stenosis

164
Q

JVP waveform - What do canon a-waves mean?

A

Extra large a waves, caused by atrial contraction against closed AV valve (tricuspid)

Compete heart block

165
Q

JVP waveform - What does c-wave correlate with?

A

Tricuspid valve closure, where it bulges back into the atria on ventricular contraction

166
Q

JVP waveform - what does x-wave mean?

A

x-descent

When ventricles contract they pull the atria down = decreased atrial pressure

167
Q

JVP waveform - what does v-wave correspond to?

When might you see prominent V waves?

A

Passive atrial filling, increasing the atrial pressure against a closed tricuspid

Tricuspid regurgitation

168
Q

JVP waveform - what is y-wave?

Why might you see a steep or shallow y-wave?

A

Y descent
opening of tricuspid and passive filling of ventricles

Shallow = tricuspid stenosis or RA myxoma 
Steep = RVF, constrictive pericarditis, tricuspid regurgitation
169
Q

ECG - what does p-wave represent?

A

Atrial depolarisation

170
Q

ECG - PR interval represent and time?

A

Time between atrial depolarisation and ventricular depolarisation
0.12-0.2 secs

171
Q

ECG - what does the QRS complex represent?

A

Ventricular depolarisation

0.06 - 0.1 secs

172
Q

ECG - what does T-wave represent ?

A

Ventricular repolarisation

173
Q

Mechanism behind inotropes?

A

Aim to increase cardiac output
Catecholamine like agents, work by increasing cAMP levels via adenylate cyclase stimulation, which causes intracellular calcium mobilisation
This causes contraction

174
Q

4 inotrope examples and the receptors they act upon?

A 
Adrenaline = lower dose beta-adrenergic, higher dose alpha receptor
Dopamine = renal and mesenteric vasodilation via D1/D2
Dobutamine = B1
Noradrenaline = A1
175
Q

How the inotropic receptors act?

A

Alpha = vasoconstriction

B1 = increased cardiac output and HR
B2 = Vasodilation
D1 = Renal and mesenteric vasodilation
D2 = inhibits noradrenaline release
176
Q

what and where are the three respiratory centres?

A

Medulla, apneustic in lower pons + pneumotaxic in upper pons

177
Q

What does each respiratory centre do?

A 
Medulla:
Inspiratory and expiratory neurones
Ventral = forced voluntary expiration
Dorsal = forced voluntary inspiration 
Depressed by opiates

Apneustic in lower pons
= stimulates inspiration - activates and prolongs

Pneumotaxic in upper pons
= Inhibits inspiration at a certain point

178
Q

Where are your respiratory chemoreceptors found?

A

Peripherally = bifurcation of the aorta and carotid body
- Respond to low PO2, H+ increased, increased CO2 in arterial blood

Central = medulla
- responds to increased H+ in the interstitial fluid of brain
NOT INFLUENCED BY OXYGEN

179
Q

Structure of haem?

What an iron bind to?

A

Protoporphyrin ring surrounding an iron atom

Iron an form two additional bonds - one with oxygen one with polypeptide chain

The polypeptide chain has 2 alpha and 2 beta subunits
Beta chains bind 2,3-DPG

180
Q

Haldane vs BOHR effet

A

Haldane = oxygen curve to the left
- means at lower oxygen levels, Hb is more saturated = delivers less oxygen

BOHR = oxygen curve to the right = for a given oxygen level there is reduced saturation of Hb. = better oxygen delivery

181
Q

What shifts the oxygen curve to the right?

A

CADET look RIGHT

CO2 increased
Acidosis
DPG increased 
Exercise
Temperature increased
182
Q

Borders of trachea?

Arterial supply?

A

C6 - T5

Inferior thyroid arteries

183
Q

Tracheostomy - what does it increase and decrease?

A

Increase = alveolar ventilation

Decrease = Work of breathing, anatomical dead space, proportion of ciliated epithelial cells

184
Q

What is functional residual capacity?
Equation?
Factors that increase it and decrease it ?

A

Volume of lung after normal expiration
FRC = RV + ERV

Decrease = upright, asthma, emphysema 
Increase = Obesity, pulmonary fibrosis, abdominal swelling, laparoscopic surgery, muscle relaxants
185
Q

When do we see high lung compliance vs low?

A

High in old people and COPD

Low = pulmonary fibrosis, lack of surfactant, atelectasis

186
Q

Alveolar ventilation - what is minute ventilation vs dead space ventilation?

A

Minute = total volume of gas ventilated per minute

Dead space = volume of gas not involved in exchange

187
Q

Anatomical vs physiological dead space?

A

Anatomical = air not involved that sits in mouth, pharynx, trachea and bronchioles
Measured by fowlers method = inhale 100% oxygen, then measure nitrogen coming out
Increased in tall people, big people, bronchodilator people

Physiological is the gas not exchanged at alveoli
Increased in COPD, PE, hypotension

188
Q

What is transfer factor?

A

Rate at which gas diffuses into alveoli

Result an be given as total gas transfer = TLCO

189
Q

What affects TLCO?

A 
Raised:
Asthma
Pulmonary haemorrhage 
L to R cardia shunts 
Polycythaemia
Male and exercise
Decreased = 
pulmonary fibrosis/oedema/emboli 
Pneumonia
Anaemia
Emphysema
Low cardiac output
190
Q

Obstructive vs restrictive lung spirometry?

A 
Obstructive = reduced FEV1, with normal / low FV
FEV1:FVC = <70% LOW

Restrictive FEV1 normal, FVC low
FEV1:FVC >70%

191
Q

Obstructive vs restrictive lung conditions?

A

Obstructive = Asthma, COPD, bronchiectasis

Restrictive = Pulmonary fibrosis, asbestosis, sarcoidosis, ARDS, kyphoscoliosis and neuromuscular disorders

192
Q

Primary peristalsis vs secondary?

A

Primary is movement from oesophagus to stomach

Secondary = Food doesn’t enter the stomach stimulates stretch receptors = peristalsis

193
Q

Of GI tract which has highest secretion go bicarb?

A

Pancreas at 115

194
Q

Of GI tract what secretes the most chloride?

A

Stomach, then jejunum/ileum, then from the bile

195
Q

Which part of GI that secretes the most potassium?

A

Duodenum

196
Q

Salivary gland through to colon volume of secretions per day?

A 
SG = 1.5L
Stomach = 1.5L
Duodenum = up to 2L
Pancreas 1L
Bile 500ml - 1L
Jejunum / ileum 3L
Colon 100ml
197
Q

In vomiting why do you get hypokalaemia?

A

Due to renal wasting

Volume of K secretion is very low ins stomach, so hypokalaemia is not due to the vomiting itself

198
Q

Ileostomy effluent?

A

22mmol/L K, 126 sodium

199
Q

Gastric secretions - what do chief cells, surface mucosal cells and parietal cells secrete?

A

Chief cells = Pepsinogen
Mucosal cells = Mucous and bicarb
Parietal cells = Mg, Ca, Na, HCL + intrinsic factor

200
Q

Phases of gastric acid secretion?

A
  1. Cephalic phase = smell and taste
    30% acid produced
    Vagal cholinergic stimulation = HCL + gastrin from G cells
  2. Gastric phase = stomach distension
    60% of acid
    Stomach distension / low pH / peptides = GASTRIN RELEASE
  3. Intestinal phase = food in duodenum
    10% of acid produced
    High acidity / distension / hypertonic solution in duodenum inhibits gastrin release via enterogastrones = CCK + secretin
201
Q

What increases / decreases gastric acid secretion?

A

Increase = vagal stimulation, gastrin and histamine release

Decrease = CKK, secretin and somatostatin

202
Q

Gastrin. - source, stimulus, inhibition and action?

A

G cells of antrum
Stimulus = distension and extrinsic
Inhibition = low pH and somatostatin

Action:

  1. Increase HCL, pepsinogen and IF secretion
  2. Cause histamine release from enterochromaffin cells
  3. Increase gut motility
  4. Trophic effect on gastric mucosa
203
Q

Cholecystokinin (CKK) - source, stimulus and action?

A

I cells from upper intestine
Stimulus = partially digested proteins and triglycerides

Action:

  1. Increase enzyme rich pancreatic secretions
  2. Contraction of gall bladder and relaxation of sphincter of Oddi
  3. Decreases gastric emptying
  4. Trophic effect on acinar pancreatic cells
  5. Induces satiety
204
Q

Secretin - source, stimulus and action?

A

S cells in upper small intestine

Acidic chime and fatty acids

Actions:

  1. Increased bicarbonate rich secretion from pancreas and hepatic duct cells
  2. Decreased gastric acid secretion.
  3. Trophic effect on pancreatic acinar cells
205
Q

VIP - source, stimulus, action?

A

Cells in upper intestine / pancreas

Neural stimulation

Action:

  1. Decreases gastric acid secretion + pepsinogen
  2. Stimulates pancreatic and intestine secretions
206
Q

Somatostatin - source, stimulus and action?

A

D cells from pancreas and stomach enterochromaffin cells

Stimulus = bile salts, fats and glucose in intestinal lumen

Action:

  1. Decreases insulin and glucagon
  2. decreases gastrin, pepsinogen and acid secretion
  3. Stops pancreatic secretions
  4. inhibits trophic effect of gastrin
  5. stimulates mucous production
207
Q

Leptin vs grehlin?

A

Leptin produced by adipose tissue, induces satiety.
Stimulates MSH and CRH

Grehlin induces hunger, produced by fundus of stomach

208
Q

Factors that increase gastric emptying?

A

Neuronal = mediated via vagus

Hormonal = gastrin

209
Q

Factors that decrease gastric emptying?

A

Hormonal = Gastric inhibitory peptide, CKK, enteroglucagon

Iatrogenic = vagotomy or distal gastrectomy
In distal gastrectomy a posteiror retrocolic anastomoses empties better vs anterior

Diabetic gastroparesis = vagus neuropathy
- means metoclopramide won’t work as this affects vagus

Malignancy = stomach or pancreas

Pyloric stenosis

210
Q

How would a somatostatinoma present ?

A

steatorrhoea
Diabetes mellitus
Gallstones

211
Q

SE’s post gastrectomy?

A

Fast passage of food = abdo pain, diarrhoea and hypoglycaemia

Iron and B12 malabsorption
Osteoporosis

Mx = High protein, low carb diet
Replace B12, iron and calcium

212
Q

Iron - where is it absorbed, how much gets absorbed, factors affecting absorption, how is it transported and stored, how is it excreted?

A

Absorbed in duodenum and upper jejunum
10% gets absorbed

Increased absorption = vitamin C and gastrin
Decreased = PPI’s, tetracycline and tannin

Transported as Fe3+ bound to transferrin
Stored in ferritin in the BM

Excreted via intestinal tract

213
Q

Ileum vs jejunum?

A

Ileum = one lucky cookie and has double layer of arcades
Also has more mesenteric fat
Thinner walled

214
Q

Role of ileum ?

what would happen in resection and Mx?

A

Absorption of vitamin B12 and bile salts
Neuroendocrine cells release hormones

Risk of bile salt malabsorption
Diarrhoea and stones
Lack of B12 predisposes to macrocytic anaemia
Mx = cholestyramine

215
Q

Pancreatic exocrine cells: Acinar vs ductal?

A 
Acinar = enzymatic
Trypsinogen
Amylase
Procarboxylase
Elastase

Ductal = aqueous secretion
Sodium, bicarb, water K and chloride

216
Q

Regulation of pancreatic exocrine secretion?

A

Digested material = CKK and Ach = stimulates ductal and acinar = enzymes etc
CKK most potent
Ductal cells also stimulated by secretion from S cells in upper duodenum

217
Q

Bile - how much produced per day, what makes up bile?

A

500ml - 1500ml

Bile salts, bicarb, steroids, cholesterol and water

218
Q

Bile salts - Reabsorption, primary vs secondary?

A

90% reabsorbed in terminal ileum to the liver

Primary = chelate and chenodeoxycholate
Secondary = Bacterial action on the primary ones = deoxycholate and lithocholate
Deoxycholate reabsorbed
Lithocholate excreted

219
Q

Which is the active thyroid hormone?

A

T3

220
Q

How are T3/T4 formed?

A

Thyroid actively concentrates iodine, this is then oxidised by peroxidase in follicular cells > atoms iodine
This then iodinates tyrosine residue in thyroglobulin

Iodinated tyrosine undergoes coupling > T3/T4

221
Q

Which cells secrete PTH?

A

Chief cells of the parathyroid gland

222
Q

Effect of PTH?

A
  1. active reabsorption of calcium. and magnesium from DCT
  2. Increases activation of vitamin D = increased intestinal reabsorption of calcium
  3. Binds osteoclast = resorption of bone
223
Q

Pancreatic endocrine function?

A

B cells = insulin
Alpha = glucagon
Delta = somatostatin
F cells = pancreatic polypeptide

224
Q

Insulin - estruture, half life, function and production?

A

Peptide hormone from B cells

Half life = 30 minutes

Causes glucose absorption by skeletal muscle, liver and fat tissue

Pro-insulin is formed in rough ER of B cells
Cleaved to form insulin and peptide C

225
Q

What common drug can inhibit insulin release?

A

BB’s

226
Q

Glucagon - action, stimulation and inhibition?

A

increase plasma glucose levels

Stimulation:
Decreased glucose levels
Increased catecholamine or amino acids
Sympathetic nervous system 
ACh and CKK

Inhibits it:
Somatostatin
Insulin
Free fatty acids and keto acids

227
Q

Stress response to surgery - overall changes?

A

Muscle protein loss
Sodium and water retention
Suppression of anabolic steroid production
Activation of sympathetic nervous system

228
Q

Stress response to surgery - Sympathetic system, vascular endothelium and normal changes?

A

Noradrenaline from symp, adrenaline from adrenal medulla = catecholamines = HTN and tachy
Also causes bronchoconstriction, reduced gut motility. and increased glucagon

Vascular endothelium releases NO = dilation
PGE’s also induce dilation and platelet aggregation

Hormonal changes:
Decreased - insulin, testosterone and oestrogen
No change - TSH, LH + FSH
Increased - GH, prolactin, ACTH, ADH, cortisol, aldosterone and renin, glucagon

229
Q

Stress response to surgery - specific hormonal response with cortisol, ADH, insulin and GH?

A

Cortisol = increased significantly within 4-6 hours
No negative feedback = raised ACTH and cortisol
Effects:
1. Increased muscle breakdown and lipolysis
2.MR effect
3. reduced inflammatory effect
4. anti-insulin

ADH = more renin = more angiotensin = more aldosterone = sodium and water retention

Insulin - B cells inhibited by the alpha 2 adrenergic effects of catecholamines

GH = increased post surgery
Stops muscle breakdown and promotes tissue repair via insulin growth factors

230
Q

Stress response in surgery - carbohydrate, protein, lipids, salt and water + cytokines?

A

Carbs = high as no insulin and catecholamines and cortisol = gluconeogenesis and glycogenolysis
NOT GOOD AS IMPAIRS WOUND HEALING + INFECTIONS

Proteins = initially only anabolism inhibited, later severe catabolism. Amino aids used for auto phase proteins

Lipids = lipolysis and ketone production
Due to increase in catecholamines and. cortisol, with lowered insulin

Salt and water - retained due to increased ADH and renin

cytokines - IL-6 is the main one, also IL-17
Peak 12-24 hours

231
Q

Stress response to surgery. - how an we modify it?

A

Opioids - cause suppression of hypothalamus and pituitary
However at too high a dose they can prolong recovery

Good nutrition

Spinal anaesthesia = reduce glucose, ACTH, GH and cortisol

Anabolic steroids and GH can help

Normothermia - lowers metabolic rate

232
Q

Outline the RAAS?

A

Renin produced in kidney (juxtagolmerular apparatus) In response to hypotension, low sodium, catecholamines and erect posture

Renin converts angiotensinogen in liver to AT1.

ACE from lung converts AT1 > AT2

AT2 ultimately results in sodium and water retention via:

  1. acts on arterioles = vasoconstriction
  2. Acts on pituitary to release ADH = collecting duct water reabsorption
  3. Increases sympathetic activity
  4. Causes aldosterone secretion = tubular Na and water retention
233
Q

Factors stimulating and inhibiting renin production?

A 
Increasing:
Low sodium
Hypotension
Erect posture
Catecholamines

Decreasing = BB’s and NSAIDs

234
Q

Glomerular function?

A

Filter

Basement membrane has poor allows smaller molecules to freely diffuse, larger -ve molecules e.g. albumin cannot

235
Q

Typical GFR, equation?

A

125mls/min

(Conc. of solute in urine x volume of urine in. 1 min) / Plasma conc.

236
Q

Where is calcium reabsorbed in the kidney?

A

DCT under the effect of PTH

237
Q

The nephron - PCT main role and what is reabsorbed / excreted?

A

Main role if reabsorption of filtrate

Reabsorbs = 100% amino acids + glucose, 65% Na + H20, 90% of HCO3
BICARB reabsorbed via the HCO3

Excretes - urea and organic acids e.g. antibiotics

238
Q

The nephron - role of loop of Henle?

A

Concentration of urine

Thin descending. limb = water reabsorption as highly water permeable. Creates gradient

Thick ascending limb = reabsorbs NACl

239
Q

The nephron - DCT role and what is absorbed / excreted?

A

pH and calcium reabsorption

Calcium reabsorbed under affect of PTH here
Sodium and water also reabsorbed

240
Q

The nephron - Collecting duct role and what acts here?

A

Water and K regulation

Na reabsorption coupled with K/H excretion
Aldosterone sensitive Na/K pump here

Also have aquaporin 2 channels controlled via ADH

241
Q

How do carbonic anhydrase inhibitors work, an example, SE’s?

A

Block the reabsorption of carbon anhydrase in PCT, and thus. small amount of Na

Acetazolamide

SE’s = metabolic acidosis, stones, ataxia

242
Q

How do loop diuretics work and SE’s?

A

e.g. furosemide

Block the Na/K/Cl transporter in thick ascending limb of loop of Henle
= excrete NaCl (also lose K and Ca)

SE’s = hypokalaemia, metabolic acidosis and ototoxic

243
Q

How do thiazides work and SE’s?

What condition should you not use thiazides in?

A

Block the NaCl transporter in DCT = more excretion
Causes more calcium reabsorption

SE’s = hypokalaemia, hyperglycaemia and increased urate

Don’t use in gout

244
Q

K sparing diuretics - 2 examples and SE’s?

A

Spiro = aldosterone antagonist
Aldosterone usually causes K excretion for Na reabsorption

Amiloride = blocks the luminal Na channel in DCT and CD

SE’s = hyperkalaemia and anti-androgenic = gynaecomastia

245
Q

What cells produce catecholamines in the adrenal medulla, and what nerves innervate them?

A

Chromaffin cells secrete noradrenaline and adrenaline

Innervated by splanchnic nerve:
- preganglionic sympathetic fibres secrete Ach causing chromatin cells to exocytose contents

246
Q

Structure of adrenal cortex?

What excretes the two products of the G and F

A

GFR
Glomerulosa = aldosterone
Fasciculata = glucocorticoids
Reticularis = androgens

Liver excretes glucocorticoids and aldosterone

247
Q

What are corticosteroids made from and how do they exert their effect?

Corticosteroids affects?

A

Synthesised from cholesterol in the adrenal cortex
Act upon specific intracellular receptor in the nucleus = affects gene transcription

Metabolic = gluconeogenesis and decreased uptake of glucose, protein breakdown and lipolysis

Regulatory = -ve feedback to hypothalamus, decreased vasodilation, osteoclast activity increased and subdues inflammation

248
Q

Adrenaline affects?

A

Alpha receptors = decreased insulin production, stimulate glycogenolysis and glycolysis

B receptors = stimulate glucagon, ACTH and lipolysis

249
Q

Renal stones - calcium oxalate: radiography and RF’s?

A

Radio-opaque

Hypercalciuria is big RF

250
Q

Renal stones - cystine - mechanism, classic features?

A

Inherited recessive disorder of transmembrane cystine transport = decreased absorption from intestine and kidneys

Multiple stones

Radio-dense as contain sulphur

251
Q

Renal stones uric acid - Mechanism, RF’s, stones?

A

Product of purine metabolism

Low urinary pH, disease with extensive tissue loss e.g. malignancy

Radiolucent stones

252
Q

Renal stones - calcium phosphate - causes and stones?

A

May occur in RTA, specifically type 1 and 3
High urinary pH

Radio-opaque

253
Q

Renal stones - struvite - what makes them up, mechanism and stone?

A

Ammonium, magnesium and phosphate = staghorn
Due to urease producing bacteria = chronic infection = proteus mirabilis

Under alkaline conditions - crystals

Radio-opaque

254
Q

Clinical features of low sodium ?

A

confusion, irritability and headache

Severe = Seizures + coma

255
Q

Classification of low sodium?

A

Based on fluid status

256
Q

Hypovolaemic hyponatraemia?

A

You lose Na and H20, but reabsorb mainly H20 with ADH
PC = postural drop, thirst + tachycardia

Urinary na >20 = renal = Thiazides or salt losing nephropathy

Urinary Na < 20 = extra renal = D+V, burns, fistula

257
Q

Euvolaemic hyponatraemia?

A

SIADH e.g. lung cancer, meningitis, head trauma, drugs e.g. sulphonylureas and SSRI’s
Urine osmolality > 500

Adrenal insufficiency = Addisons = low cortisol = lBP = ADH release

Hypothyroid = reduced heart contractility = reduced CO = ADH release

258
Q

Hypervolaemic hyponatraemia?

A

Raised JVP, bibasal creps + oedema

Heart failure = low BP = ADH
Liver cirrhosis = NO release = vasodilation = BP drops = ADH release

Kidney failure

Commonly seen in surgery due to overuse of IV dextrose

259
Q

Hypernatraemia - causes, Ix and Mx

A

Usually due to dehydration
- Unreplaced water loss = GI losses, diabetes diuresis or DI

Ix:
Check blood sugars for diabetes
Check urine osmolality - if >700 excludes DI
Water deprivation test - if still can’t concentrate urine = DI

Give Desmopressin - if helps =. cranial, if doesn’t work = nephrogenic

Mx = IV dextrose

260
Q

lab features of dehydration ?

A 
Hypernatraemia
Raised haematocrit 
Creatinine up
Urinary sodium > 20
Metabolic acidosis
Lactate high
Urine osmolality increased
261
Q

Hypokalaemia - clinical features and specific ECG changes?

A

Tetany and cramps
Muscle weakness, hyporeflexia
Arrhythmias

ECG - Flattened T-waves, prominent u-waves, long PR interval

262
Q

Hypokalaemia 4 causes?

A
  1. Renal loss = RTA, thiazides / Gittlemans + Loop/Barters
  2. GI loss
  3. Excess aldosterone - Conns
  4. Redistribution - Salbutamol, insulin
263
Q

Mx of hypokalaemia?

A

3-3.5 = oral KCL, recheck

<3 = IV KCL, max 10mmol/hour

Treat cause

264
Q

Clinical features of hyperkalaemia and specific ECG changes?

A

Palpitates, chest pain and weakness

ECG = Tented T waves, flattened P waves, broad QRS

265
Q

Causes of hyperkalaemia?

A
  1. Renal:
    - Low eGFR = no filter > basically any cause of renal disease then
    - RTA
  2. Drugs = NSAIDS, ACEI, ARBS, spiro (also heparin and ciprofloxacin)
  3. low aldosterone = Addisons
  4. cellular redistribution = rhabdomyolysis e.g. burns, any acidosis
  5. Massive transfusion
266
Q

Mx of hyperkalaemia?

A

10ml 10% calcium glucoate
50ml 50%dextrose + 10IU of insulin
Salbutamol nebs

267
Q

How does PTH increase calcium?

A
  1. via activating 1,25-(OH)2.D
    = Increases bowel reabsorption and renal reabsorption
    = Osteoclastic activity at high levels

PTH does not directly bid to osteoclasts, but sends signal via osteoblasts

268
Q

What might happen to PTH levels post parathyroid surgery?

A

Drop = hypocalcaemia
Neuromuscular irritability + laryngospasm

Give calcium gluconate ASAP

269
Q

What cells produce calcite and how does it work?

A

Secreted by thyroid C cells

Inhibits:
Intestinal reabsorption
Osteoclast activity
Renal tubular reabsorption

270
Q

Causes of low calcium?

A

PTH driven = low PTH:
Autoimmune hypoparathyroid
Di Georges = Cleft palate, abnormal facies, thymus aplasia, cardiac, hypocalcaemia, Chr 22

not PTH driven = high/normal
= Vitamin D low, chrnic renal failure, malabsorption

271
Q

Features of low calcium?

A

Muscle spasm, seizure, chvosteks/trousseaus

272
Q

How does albumin affect calcium?

A

Calcium bound to albumin > Low albumin = low calcium

Alkalosis = albumin protonation. = low calcium

273
Q

Dystrophic calcification vs metastatic?

A

Dystrophic = calcium deposits in tissues that have undergone damage / degeneration
Normal serum calcium levels
e.g. breast cancer

Metastatic = normal tissue, high serum calcium

274
Q

Hypomagnesaemia - Causes and features?

A 
Causes:
Diuretics
TPN
Low calcium and K
Diarrhoea
Alcohol

Features = Paraesthesia, tetany, seizures, arrhythmias, reduced PTH

275
Q

How are calcium and mg linked?

A

Low magnesium can cause low PTH and means it cannot act on target cells

276
Q

Hyperuricaemia - causes?

A

Either increased synthesis or decreased excretion

277
Q

What causes increased synthesis of uric acid?

A 
Lesch-Nyhan
Myeloproliferative disease
Exercise
Psoriasis
Cytotoxics
278
Q

What causes decreased excretion of uric acid?

A 
Drugs = CANT LEAP
Ciclocporin
Alcohol
Nicotinic acid
Thiazides 
Loop diuretics
Ethambutol. 
Aspirin
Pyrazinamide

Pre-eclampsia
Renal failure
Lead

279
Q

Vitamin deficiency: A

A

Night blindness, epithelial atrophy and infections

280
Q

Vitamin deficiency: B1

A

Thiamine

Beri Beri
Wet = tachycardia, SOB ad leg swelling
Dry = neuro signs - can’t move legs, numbness and tingling

281
Q

Vitamin deficiency: B2

A

Dermatitis

Photosensitivity

282
Q

Vitamin deficiency: B3

A

Pellegra

3D’s = dementia, dermatitis and diarrhoea

283
Q

Vitamin deficiency: B12 - causes, features and Mx

A

causes = Pernicious anaemia, post-gastrectomy, poor diet, terminal ileal disease

Features = Macrocytic anaemia, sore tongue , neuro e.g. ataxia, neuropsychology e.g. mood

Mx = 1mg IM 6 times over two weeks, the 3 monthly
If folic acid too, replace the B12 first to avoid SCDC

284
Q

Vitamin deficiency: C

A

Poor would healing, impaired collagen synthesis

285
Q

Vitamin deficiency: D

A

Rickets / osteomalacia

286
Q

Vitamin deficiency: K

A

Clotting disorders

If jaundiced = impaired absorption

287
Q

What vitamin is needed for collagen synthesis, what cells produce collagen?

A

Vitamin C needed for hydroxylation of proline

Produced by fibroblasts

288
Q

Collagen disease - Osteogenesis imperfects types? Symptoms?

A

Defect in collagen type 1

Fractures and loose joints

Subtypes:
Type 1 = normal collagen, insufficient amounts
Type 2 = Poor quantity and quality
Type 3 = Normal quantity, poor quality
Type 4 = sufficient quantity, poor quality

289
Q

Collagen disease - ED - abnormality?

A

Abnormality in type 1 and 3

290
Q

What is refeeding syndrome?

A

poor feeding = risk of low K/Mg/PO4 = organ failure

291
Q

If not fed for >5 days, what % calories should we start at?

A

50%

292
Q

High risk of refeeding?

A

BMI <16
Weight loss >15% over 3-6 months
Little PO > 10 days
Electrolyte abnormality

293
Q

Mx of refeeding?

A

Thiamine and B12
Slowly increase PO intake
Monitor electrolytes

294
Q

In hypovolaemic shock, what urinary sign do you see?

A

Increased urine specific gravity

295
Q

Why does angiogenesis occur In wound healing?

A

Due to endothelial cell proliferation

296
Q

Which cardiovascular receptor does dobutamine show a preference for?

A

B1 cardioreceptor = increased cardiac contractility and HR

297
Q

How does T3 work?

A

Binds to nuclear receptor chromatin. = protein synthesis

298
Q

Causes of increased anion gap acidosis?

A 
MUDPILES
M - Methanol 
U - Uraemia 
D - DKA
P - Paraldehyde/phenformin 
I - Iron
L - Lactic acidosis 
E - Ethylene glycol 
S - Salicylates
299
Q

Best measure of renal plasma flow?

A

Para-amino hippuric acid (PAH)

300
Q

Does adrenaline cause coronary vasospasm?

A

No
It doesn’t affect the B2 cardiac receptors which = vasospasm
Its cardiacs effects are mediated by B1

301
Q

Causes of pseudohypernatraemia?

A

Multiple myeloma, hyperlipidaemia, high glucose

302
Q

Major functions of the spleen?

A
  1. Filtration of abnormal blood cells and foreign bodies such as bacteria.
  2. Immunity: IgM. Production of properdin, and tuftsin which help target fungi and bacteria for phagocytosis.
  3. Haematopoiesis: up to 5th month gestation or in haematological disorders.
  4. Pooling: storage of 40% platelets.
  5. Iron reutilisation
  6. Storage monocytes
303
Q

5 drugs that use pseudohaematuria?

A

Rifampicin, phenytoin, levodopa, methyldopa, and quinine

304
Q

Which amino acids are catecholamines derived from?

A

Tyrosine

MRCS A - Physiology + Pathology (2 decks)

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