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Yr 2 EOYS ^2 > MET EOYS1 > Flashcards

MET EOYS1 Flashcards

1
Q

What is A

Middle colic artery
Jejunal arteries
Ileal colic artery
Right colic artery

A

What is A

Middle colic artery
Jejunal arteries
Ileal colic artery
Right colic artery

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2
Q

Label A & B [2]

A

A Jejunal arteries
B Ileal arteries

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3
Q

Label A-E

A

A: Left colic artery
B: IMA
C: Ileal arteries
D: Ileocolic artery
E: Right colic artery

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4
Q

What is A?

Left colic artery
SMA
Middle colic artery
Ileocolic artery
Right colic artery

A

Middle colic artery

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5
Q

Which two points does the inguinal ligament run between? [2]

A

ASIS to pubic tubercle

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6
Q

Which two molecules can activate the adenylyl cyclase pathway, which causes glycogenlysis, GNG? [2]

A

Glucagon
Adrenaline

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7
Q

As the food bolus is pushed into the pharynx the epiglottis of the larynx is pulled inferiorly to prevent food being aspirated.

Which nerve is responsible for closure of the larynx?

Superior laryngeal nerve
Recurrent laryngeal nerve
Glossopharnygeal nerve
Vagus nerve

A

As the food bolus is pushed into the pharynx the epiglottis of the larynx is pulled inferiorly to prevent food being aspirated.

Which nerve is responsible for closure of the larynx?

Superior laryngeal nerve
Recurrent laryngeal nerve
Glossopharnygeal nerve
Vagus nerve

As the recurrent laryngeal nerve innervates all muscles of the larynx (except cricothyroid) it is responsible for the closure during swallowing.

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8
Q
A
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9
Q

describe the branches of the SMA (6)

A
  1. inferior pancreaticoduedenal artery
  2. jejnunal and ileal branches

3 middle colic artery

  1. right colic artery
  2. ileocolic artery -> appendicular artery

MRI !

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10
Q

Contrast-enhanced CT is performed with selected images shown. What is the most likely diagnosis?

Amyand hernia
De Garengeot hernia
femoral hernia
direct inguinal hernia
indirect inguinal hernia
obturator hernia

A

This 50-year-old man presents with abdominal pain. Abdominal x-ray shows small bowel dilatation. Contrast-enhanced CT is performed with selected images shown. What is the most likely diagnosis?

Amyand hernia
De Garengeot hernia
femoral hernia
direct inguinal hernia
indirect inguinal hernia
obturator hernia

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11
Q

Name the gene that causes polycystic kidney disease [1]

Describe the inheritance pattern [1]

A

PKD1 or PKD2

Autosomal dominant

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12
Q

Name two Calcineurin inhbitors [2]

A

Cyclosporin and tacrolimus

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13
Q

Prednisolone targets which cytokine gene activation? [1]

A

IL-2

Learn x

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14
Q

Which of the following targets IL-2 gene activation / suppresses IL-2 activation

Azathioprine
Prednisolone
Cyclosporin
Tcrolimus
Mycophenolic acid

A

Which of the following targets IL-2 gene activation / suppresses IL-2 activation

Azathioprine
Prednisolone
Cyclosporin
Tcrolimus
Mycophenolic acid

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15
Q

Immunosuppressant drugs

Which of the following are calcineurin inhibitors? [2]

Azathioprine
Prednisolone
Cyclosporin
Tacrolimus
Mycophenolic acid

A

Which of the following are calcineurin inhibitors? [2]

Azathioprine
Prednisolone
Cyclosporin
Tacrolimus
Mycophenolic acid

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16
Q

Describe the action of calcineurin [1]

A

Calcineurin is an enzyme that activates T-cells of the immune system.

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17
Q

How long should ischaemia be limited to prevent acute transplant rejection:

-Cold ischaemia? [1]
- Warm ischaemia? [1]

A

Cold ischaemia time: 12 hrs
Warm ishaemia time: 1 hour

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18
Q

Which gene causes this disease? [1]

Describe the structure that this gene predominately codes for [1]

A

Polycystin gene - codes for primary cilia

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19
Q

Conn’s syndrome causes which of the following effects

  • increase sodium reabsorption; increase potassium excretion
  • decrease sodium reabsorption; increase potassium excretion
  • decrease sodium reabsorption; decrease potassium excretion
  • decrease sodium reabsorption; decrease potassium excretion
A

Conn’s syndrome causes which of the following effects

  • increase sodium reabsorption; increase potassium excretion

Conns syndrome: XS aldosterone

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20
Q

What are the triad of signs of Conns syndrome? [3]

A

hypokalemia, hypernatremia and metabolic alkalosis

21
Q

Conns syndrome patient presents with

Respiratory alkalosis
Respiratory acidosis
Metabolic alkalosis
Metabolic acidosis

A

Conns syndrome patient presents with

Respiratory alkalosis
Respiratory acidosis
Metabolic alkalosis
Metabolic acidosis

22
Q

This symptoms is suggestive of

Conns syndrome
Cushings syndrome
Addisons disease
Sunburn

A

This symptoms is suggestive of

Conns syndrome
Cushings syndrome
Addisons disease
Sunburn

Hyperpigmentation is characteristic and occurs in almost all patients.
Elevated ACTH and melanocyte-stimulating hormone are causative factors. It is believed that ACTH binds to the melanocyte receptors, which are responsible for pigmentation

23
Q

Describe the ascent of the kidneys during development:

Where do they start from? [1]

Where do they finish? [1]

(Include vert levels)

A

Describe the ascent of the kidneys during development:

Where do they start from? [1]
Sacral region S1

Where do they finish? [1]
Lumbar region T12

(Include vert levels)

24
Q

Why wont babies survive bilateral kidney agenesis? [2]

A

If kidneys dont develop then effects creation of amniotic fluid (reduced: oligohydramnios)

This causes failure of lung development

25
Q

Describe pathophysiology of autosomal dominant polycystic kidney disease

How do cysts grow? [4]

A

Mutation on polycystin gene: involved in production in primary cilia (ciliopathy)

Primary cilia involved in cell adhesion, calcium transport and cell cycle.

Cysts growth:

  • Cysts originates as dilations of intact tubule
  • Increased proliferation of cyst epithelium
  • Cyst epithelium becomes secretory resulting in increased fluid secretion into lumen of cyst
  • Cyst enlarges and loses contact with nephron
26
Q

Which variables are used for MDRD equation to measure clearance? [4]

A

Need:
Cretinine
Age
Gender
Ethnicity

27
Q

Name and explain which transport protein in the thick ascending loop of Henle assists NaKCl2 transporter

A

Renal Outer Medullary potassium channel or ROMK

  • K is AT pumped into the tubular lumen / urine to generate positive voltage within the cell (because less K+ in)
  • This creates an overall voltage gradient of +80mV; from +10mV in the tubular lumen to -70mV in the tubular cell
  • This voltage difference drives Na into the tubular cell via NaKCl2 transporter
28
Q

what other function do macula dense cells do ? / what do they produce?

A

The macula densa cells also tonically produce prostaglandin PGE2
which acts on juxtaglomerular cells to stimulate renin release

low sodium levels = More prostaglandin = more renin

29
Q

what is the location, function and mechanism of action for the NKCC2 channels?

A

NKCC2 (Na-K-Cl cotransporter channel

  • location: thick ascending limb of the loop of Henle
  • function: to get Na / Cl out of the ascending limb and into extracellular fluid
  • mechanism of action:
    i) luminal walls of the epithelial cells allows sodium, potassium & chloride ions to move passively together down their concentration gradient into the cells that make thick ascending limb
    ii) then, sodium is actively transported out into extracellular space by Na/K ATP-ase
    iii) Cl- moves passively with the sodium
    iv) most of K+ ions diffuse back into the lumen via K ion channels

https://www.youtube.com/watch?v=sapTNUtrPdY

30
Q

How would you calculate a MUST score? [3]

How do you work out an Action Plan for MUST? [1]

A

MUST:
1. BMI
2. Weight Loss
3. Acute disease effect
4. Add scores for 1-3
5. Action Plan

31
Q

If MUAC is less than [], BMI is likely to be underweight (<20 kg/m2)

If MUAC IS over [], BMI is likely to be overweight ( >30 kg/m2)
.

A

If MUAC is under 23.5, BMI is likely to be under 20 (underweight)

If MUAC IS >32, BMI is likely to be >30 (overweight)

32
Q

It is a widely held belief that low albumin arises because of inadequate protein intake.

Explain what causes Hypoalbuminaemia in hospital? [2]

A

Cause in hospital: is inflammation and sepsis:

  • increased C-Reactive Protein
  • White Cell Count
  • pyrexia
  • infection

In these patients capillary walls become more ‘porous’ and albumin drifts out –> low plasma albumin

Low albumin often occurs in sick, malnourished patients, but it is not caused by poor intake

33
Q

Which Ptx are at risk of refeeding syndrome? [1]

Which Ptx are at high risk of refeeding syndrome? [4]

Which Ptx are at very high risk of refeeding syndrome? [4]

A

Risk
* Any ptx with very little food for more than 5 days

High risk
ONE OF:
Any one the following;
* BMI less than 16
* Unintentional weight loss >15% in last 3-6 months
* Little or no nutritional intake for more than 10 days
* Low levels of K, PO, Mg prior to feeding

Very high risk
TWO OF THE FOLLOWING:
* BMI less than 18.5
* Unintentional weight loss >10% in last 3-6 months
* Little or no nutrition for more than 5 days
* A history of alcohol abuse or drug use including chemotherapy, antacids or diuretics

34
Q

What are two mechanisms that acute rejection occurs?

A

Acute rejection can be either via:

Acute Cellular Rejection (ACR)
- Cytotoxic T lymphocyte response
- Macrophage response

OR

Acute Antibody Mediated Response (AMR)

  • B lymphocyte response making antibodies (agaisnt MHC Class 1 /2 antigens or ABO blood group antigens)
35
Q

Antibody-mediated rejection (AMR):

What are the main antigens targets of antibodies? [3]
Where does this mainly occur? [1]

A

Antibody targets:
* MHC (Class I & II): HLA antigens:
* ABO antigens
* MHC class I-related chain A (MICA)

Target location: endothelium - targets arteries and capillaries (because these are the cells first meet after transplantation)

36
Q

With regards to acute rejection of transplants, how would you detect antibody prescence?

A

Detect antibody presence with complement: C4d

  • The antibody-antigen complex activates the compliment system
  • This produces C4d molecules (which forms covalent bonds with endothelial cells)
  • C4d molecules are stained easily
  • This shows that acute rejection has occurred

Staining for C4d is a very good proxy for detecting antibodies

37
Q

What is criteria for diagnosis of acute antibody rejection? [3]

A

Evidence of acute renal injury on histology (often microvascular inflammation)

Evidence of antibody activity C4d staining in peritubular capillaries

Circulating anti-donor specific antibodies

38
Q

Explain how AMR causes damage in hyperacute rejection

A

change from anti-coagulant to pro-coagulant state:

  • antibodies bind to surface of epithelial cells: become pro-coagulant and clots form
  • causes downstream infarction
  • causes haem.
39
Q

Summary of hyperacute rejection:

Within 1 hr you get [] infiltrate of peritubular capillaries

Within 12-24 hrs you get what effects? [2]

A

Within 1 hr you get neutrophils infiltrate of peritubular capillaries

Within 12-24 hrs you get intravascular coagulation and cortical necrosis

40
Q

How can we prevent hyperacute rejection? [3]

A
  1. Use somone who is ABO compatabile (O is universal donor)
  2. screen for preformed antibodies:
    * Direct cross match: mix donor cells and recipient serum. Look for complement activation (positive is bad)
    * Beads with bound HLA: look to see if recipient serum binds to HLA beads
41
Q

What are the most important HLAs? [3]

A

HLA A
HLA B
HLA DR

Each have two genes

42
Q

Explain how can you prevent acute rejection of transplants? [2]

A

HLA matching (make sure that not positive for match)

Minimising ischaemia-reperfusion injury:

  • Ischaemia causes upregulation of adhesion molecules, which increases adhesion of leukocytes when blood is reperfused.
  • More leukocytes increases chance of rejection, SO try and limit ischaemia time.
  • Cold ischaemia time: 12 hrs
  • Warm ishaemia time: 1 hour
43
Q

What are the two pathways of allorecognition?

A

Direct:
* Recipient T-cells recognise allogenic APC (donor APCs) and cause aggressive imune response to foreign HLA

Indirect:
* The allogenic APCs are replaced with auto-APCs
* Some of the peptides presented by new auto-APCS are derived from shed HLA molecules
* Causes a more gentle immune response

44
Q

Explain how activation of a helper T cell / CD4 cell occurs [3]

A
  1. T helper cell receptor recognising antigen from HLA
  2. Co-stimulation from another molecule

Both these signals activate nucleus to make IL-2.

IL-2 binds to IL-2 receptor on different T helper cell. [3]

Causes signal at nucleus to make proliferation of T-helper cells

45
Q

What are the sites of action used for immunosuppressive drugs? [3] and what drugs used?

A

Calcineurin inhibitors:
* Calcineurin is an enzyme that activates T-cells of the immune system.
* E.g. Cyclosporin and tacrolimus (learn !)

Anti-proliferative drugs:
* (target nucleus at end stage of T cell activation)
* e.g. Azathioprine and Mycophenolic acid

Prevent cytokine (IL-2) gene activation
* Use cortiosteroids
* e.g. Prednisolone

Standard treatment: Calcineurin inhib, steroid and anti-proliferative drugs

46
Q

Label A & B of developing kidneys

A

A: mesonephric bud
B: uteric bud

47
Q

What type of renal pathology is depicted here?

IgA neuropathy
Membrane change disease
Glomerulonephritis
Acute rejection from kidney transplant

A

What type of renal pathology is depicted here?

IgA neuropathy
Membrane change disease
Glomerulonephritis
Acute rejection from kidney transplant
Focal glomerulitis in active antibody mediated rejection-Banff score g3. Dilated glomerular capillaries are filled with swollen endothelial cells and inflammatory cells (PAS, 200×).

48
Q

GPR54 is involved in the stimulation of which pituitary hormone? [1]

GPR101 is involved in the stimulation of which pituitary hormone? [1]

A

GPR54: GnRH

GPR101: Growth Hormone

49
Q

A woman is admitted with left-sided weakness and collapse. She is brought in with her husband, who explains that she has no drug allergies and a past medical history of diabetes, hyperthyroidism and autosomal dominant polycystic kidney disease.

A CT scan of the head shows a large, right-sided intracerebral bleed.

What is the most likely cause of the bleed?

Hypertension
Poorly controlled diabetes
Ruptured berry aneurysm
Atherosclerotic disease
Paradoxical embolism

A

Ruptured berry aneurysm
Adult polycystic kidney disease increases the risk of brain haemorrhage due to ruptured berry aneurysms

Yr 2 EOYS ^2 (42 decks)

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