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Yr 2 EOYS > MET EOYS4 > Flashcards

MET EOYS4 Flashcards

1
Q

Which of the following is not associated with obesity causing a dampened down immune system?

RA
MS
Systemic lupus erythematosus
Psoriasis

A

Which of the following is not associated with obesity causing a dampened down immune system?

RA
MS
Systemic lupus erythematosus
Psoriasis

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2
Q

A Ptx present with greater span than height & shorter 4th metacarpal. Which of the following is most likely

McCune-Albright Syndrome
Patau Syndrome
Kallman Syndrome
Turners Syndrome

A

A Ptx present with greater span than height & shorter 4th metacarpal. Which of the following is most likely

McCune-Albright Syndrome
Patau Syndrome
Kallman Syndrome
Turners Syndrome

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3
Q

McCune-Albright syndrome is caused by a mutation on which gene

Kal
GNAS
PIT1
GSP

A

McCune-Albright syndrome is caused by a mutation on which gene

Kal
GNAS
PIT1
GSP

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4
Q

Diabetic nephropathy causes the creation of which structures in the glomerulus? [1]

A

Kimmelstiel–Wilson nodules

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5
Q

Where does spirolactone work?

PCT
LoH
DCT
CD

A

Where does spirolactone work?

PCT
LoH
DCT
CD

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6
Q

What effect do SGLT-2 inhibitors have on afferent and efferent arterioles? [2]

A

Vasoconstriction at afferent arteriole

No effect at efferent (i think)

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7
Q

Which of the following has neuron development through the cribiform plate?

GnRH
TRH
CRH
ADH

A

Which of the following has neuron development through the cribiform plate?

GnRH
TRH
CRH
ADH

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8
Q

hypothalamic stimulating hormone that causes the release of GnRH

somatostatin
PIT1
kisspeptin
GPR54

A

hypothalamic stimulating hormone that causes the release of GnRH

somatostatin
PIT1
kisspeptin
GPR54

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9
Q

Which of the following is the nerve that causes constriction of the pupil?

A
B
C
D
E

A

Which of the following is the nerve that causes constriction of the pupil?

A: CN 3
B
C
D
E

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10
Q

Which of the following is the ophthalmic branch is the first division of the trigeminal nerve?

A
B
C
D
E

A

Which of the following is the ophthalmic branch is the first division of the trigeminal nerve?

A
B
C
D
E

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11
Q

Which of the following supplies the lateral rectus?

A
B
C
D
E

A

Which of the following supplies the lateral rectus?

A
B
C
D
E

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12
Q

Which pituitary hormone binding to cell surface-localize receptors (GHRs) induces a conformational change of the dimerized receptors?

CRH
TSH
GH
ADH

A

Which pituitary hormone binding to cell surface-localize receptors (GHRs) induces a conformational change of the dimerized receptors?

CRH
TSH
GH
ADH

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13
Q

Name the hypothalamic stimulating hormone that causes the release of GnRH [1]

A

Kisspeptin

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14
Q

Explain oestrogen positive feedback of puberty cycle for LH / FSH

A

Gonad makes oestrogen, which has a positve effect on kisspeptin via GPR54 receptor

Kisspeptin neurones stimulate GnRH

GnRH stimulates gonadotrophs, which makes LH & FSH

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15
Q

Describe path of GnRH neurone formation

What two phenotypes that occur if this process occurs innappropiately [2]

A

GnRH neurones develop in the olfactory epithelium.

During embryonic development GnRH neurones migrate through cribiform plate, guided by Kal protein & migrate to the hypothalamus

(neurones migrate with cells responsible for smell but go to olfactory bulb not the hypothalamus)

Causes a lack of smell and hypogonadism

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16
Q

Describe pathphysiology of Kallman syndrome [3]

A

Mutation in Kal protein [1]

During embryonic development these cells can’t enter brain: doesnt take neurones to hypothalamus / olfactory bulb

Cross stalk between two sides of the brain is innappropriate (so cant do movements with one hand indivdually)

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17
Q

How would you test for Kallman syndrome? [2]

A

Have shorter 4th metacarpal:

Test by putting pencil between small finger and middle finger metacarpal:

  • Normal person the pencil wont touch if placed there
  • Does in Kallman syndrome

Also: have greater span than height

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18
Q

Label the different cranial nerves present in cavernous sinus

A
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19
Q

The anterior pituitary reqiures which transcription factors to develop? [1]

A

PIT1 [1]

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20
Q

What are developmental consequences of being deficient in PIT1? [2]

A

Hypothyroidism develops to create cretinism

Overall lacks TSH,GH and Prolactin

21
Q

Label A-F

A
22
Q

What type of receptor is GHRH receptor? [1]

Explain what happens when GHRH receptor is activated [2]

A

GPCR

Alpha subunit:
- cuts off a phosphate / hydrolises GTP to GDP which originally activated the alpha subunit (regulatory step: so that adenylyl cyclase isnt continually switched on

  • activates adenylyl cyclase, which creates cAMP: second messenger to activte GH
23
Q

Explain effect of gsp oncogene with regards to GHRH receptor and human pituitary tumours [1]

A

GSP oncogene:

Causes a mutant alpha subunit:
- cannot hydrolise GTP to GDP, which results with alpha subunit constantly activating adenylyl cyclase

24
Q

Which syndrome is created by a mosaic mutation in GNAS gene? [1]

How do they present? [4]

A

McCune-Albright syndrome

(Cannot be inherited)

Syndrome has classic traid of:
* polyostotic fibrous dysplasia of bone
* precocious puberty
* café-au-lait skin pigmentation
* Acromegaly is seen in about 20% of patients with MA

25
Q

How does GH bind to GH receptor?

A

Binding of GH to its receptor results in dimerization of the GHR: causes intra-cellular spinning of the receptor

26
Q

Fill in the blanks for production of FSH & LH

A

A: Kisspeptin
B: GPR54
C: GnRH

27
Q
A
28
Q

What is the most common cause of ACTH-indepedent Cushing’s syndrome? [1]

Name two other causes

A

Exogenous glucocorticoid threapy (steroid therapy)
(e.g. long term inhaler use)

Can be due to adrenal hyperplasia or adrenal tumour

29
Q

Thiazide diuretics work in which location of nephron? [1]

MoA of thiazide diuretics? [1]

A

Thiazide diuretics: work at DCT

MoA: Blocks Na/Cl transporter

30
Q

Where do potassium sparing diuretics, such as spironolactone or eplerenonework in nephron? [1]

MoA? [1]
How do they ensure K+ reabsorption? [1]

A

Spironolactone and eplerenone work at CD

Both: aldosterone antagonists (Na/K transporter)

Because Na doesn’t get reabsorbed into blood, K doesn’t have to be excreted in exchange

31
Q

Explain two AEs of using loop diuretics? [3]

A

Hypokalemia: directly blocks K reabsorption through blockage of NaKCl2

Dehydration

Kidney stones: due to retained Ca in urine

Deafness

32
Q

What are clinical uses of aldosterone inhibitors? [4]

A

Hyperaldosteronism (Conns)
Heart failure
Hypokalaemia (from other diuretics)
Cirrhosis

33
Q

AEs of aldosterone inhibitors? [3]

A

Hyperkalaemia
Hyperkalaemia –> can lead to cardiac arrythmias and death
Hyperkalaemia
Gynecomastia (not eplerenone)
Hyponatraemia (Cirrhosis)

34
Q

When would you use osmotic diuretic clinically? [1]

A

Clinical use:
* Cerebral odema

AEs:
* Transient fluid overload: pulmonary odema
* If using glucose: DKA/HHS
* If using urea: Disequilibrium syndrome

35
Q

Explain MoA of SGLT-2 inhibitors

A

Normally SGLT2 allows Na AND glucose to be reabsorbed at PCT

Blocking SGLT2 causes more Na to be delivered to macula densa: here it causes glomerulus afferent arteriole constriction, which normalises GFR. Also causes glucose to be excreted in urine

36
Q

How can you distinguish that cells are from the CD?

A
  • prominent lateral borders of the epithelial cells
  • Cytoplasm of collecting duct cells is relatively clear (i.e., not as intensely eosinophilic as that of proximal or distal tubules)
  • and cell borders are usually distinct.
37
Q

Describe the different layers of the ureter [3]

A
  • an inner longitudinal layer smooth muscle
  • an outer circular layer of smooth muscle
  • lumen of the ureter is covered by transitional epithelium
38
Q

Describe pathophysiology of minimal change disease

A

Glomerulus appears norma under light microscopel but under electron microscope: loss of foot processes of the podocytes and glomerular filtration barrier

Loss of albumin: causes peripheral oedema, pitting oedema, puffy face and overall unwell

39
Q

Describe pathophysiology of diabetic nephropathy

A
  • Linked to high glucose
  • Caused by thickening of basement membrane and matrix: causes stretching of podocytes and endothelial cells
  • this creates Kimmelstiel–Wilson nodules
  • creates micro-aneursyms: more likely to get blood plasma and albumin in the filtrate
  • finally causes lipohyaline cap deposits and hyalinosis of afferent and efferent arterioles (concentric hyaline thickening of the cerebral small vessels)
  • the chronic high level of glucose passing through the glomerulus causes scarring. This is called glomerulosclerosis
40
Q

Describe pathophysiology of primary Glomerulonephritis

  • What is it caused by? [2]
  • What happens to structure of glomerulus? [3]
A

Glomerulonephritis is an umbrella term applied to conditions that cause inflammation of or around the glomerulus and nephron.

  • Membranous glomerulonephritis characterised by thickening of glomerular basement membrane due to presence of subepithelial immune deposits
  • can be caused autoimmune pathology: autoimmune disease systemic lupus erythematosus (SLE) and production of self antigen antibodies such as anti-phospholipase A2 antibodies being deposited in the kidney:
  • The deposition of the immune complex at the glomerular membrane is responsible for the inflammatory reaction at the glomerulus
41
Q

Obesity and comorbidities:

Name 4 impacts of immunity because of obesity

A

Obesity induces a dysregulated immune system which can be seen from childhood.

Increased susceptibility to range of infections:
* surgical-site
* urinary tract
* nosocomial
* skin

Impaired response to vaccines

Evidence linking obesity with:
* Rheumatoid arthritis
* Multiple Sclerosis
* Psoriasis and Psoriatric Arthritis

42
Q

Visceral Fat Measurement in Practice:

healthy central adiposity: waist-to-height ratio [] to [], indicating no increased health risks

increased central adiposity: waist-to-height ratio [] to [], indicating increased health risks

high central adiposity: waist-to-height ratio [] or more, indicating further increased health risks.

A

Visceral Fat Measurement in Practice:

healthy central adiposity: waist-to-height ratio 0.4 to 0.49, indicating no increased health risks

increased central adiposity: waist-to-height ratio 0.5 to 0.59 indicating increased health risks

high central adiposity: waist-to-height ratio 0.6 or more, indicating further increased health risks

43
Q

Which pathology is depicted using immunohistocomplex staining?

IgA nephropathy
Membranous change disease
DIabetic nephropathy
Glomerulosclerosis

A

Which pathology is depicted using immunohistocomplex staining?

IgA nephropathy
Membranous change disease
DIabetic nephropathy
Glomerulosclerosis

44
Q

Which pathology is depicted using immunohistocomplex staining?

IgA nephropathy
Membranous change disease
DIabetic nephropathy
Glomerulosclerosis

A

Which pathology is depicted using immunohistocomplex staining?

IgA nephropathy Proliferation and hypercellularity of the mesangium is seen in the glomerulus
Membranous change disease
DIabetic nephropathy
Glomerulosclerosis

45
Q

Which pathology is depicted in this histology slide?

IgA nephropathy
Membranous change disease
DIabetic nephropathy
Glomerulosclerosis

A

Which pathology is depicted using immunohistocomplex staining?

IgA nephropathy
Membranous change disease
DIabetic nephropathy Staining of the lipohyaline caps with periodic acid Schiff stain. Note the subendothelial location of the deposits filling the capillary lumina.

46
Q

Which pathology is depicted in this histology slide?

IgA nephropathy
Membranous change disease
DIabetic nephropathy
Glomerulosclerosis

A

Which pathology is depicted using immunohistocomplex staining?

IgA nephropathy
Membranous change disease
DIabetic nephropathy - note the Kimmelstiel-Wilson nodules
Glomerulosclerosis

47
Q

Which pathology is depicted in this histology slide ?

IgA nephropathy
Membranous change disease
DIabetic nephropathy
Glomerulosclerosis

A

Which pathology is depicted using immunohistocomplex staining?

IgA nephropathy - mesengial hypercellulairty
Membranous change disease
DIabetic nephropathy
Glomerulosclerosis

48
Q

Which pathology is depicted using slide?

IgA nephropathy
Membranous change disease
DIabetic nephropathy
Glomerulosclerosis

A

Which pathology is depicted using immunohistocomplex staining?

IgA nephropathy
Membranous change disease
DIabetic nephropathy
Glomerulosclerosis

Yr 2 EOYS (58 decks)

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