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MET2 > MET2 Revision 6 > Flashcards

MET2 Revision 6 Flashcards

1
Q

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

A

Kisspeptin

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2
Q

What do you need to remember about the structure of TSH, LH, FSH & HCG? [1]

A

Have same alpha subunit; different beta subunit

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3
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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4
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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5
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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6
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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7
Q

Role of oxytocin? [4]

A

Giving birth, milk ejection

Social recognition
– “love hormone”

Pro-sociality
– For and maintain attachment bonds with others

Perceptual selectivity/social salience
– intranasal oxytocin increases gaze to the eye region

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8
Q

Label the different cranial nerves present in cavernous sinus

A
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9
Q

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

A

PIT1 [1]

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10
Q

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

A

Hypothyroidism develops to create cretinism

Overall lacks TSH,GH and Prolactin

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11
Q

Label A-F

A
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12
Q

Roles of GHRH? [4]

A
  1. Stimulates GH release
  2. Stimulates GH synthesis
  3. Increases GH cell number
  4. Promotes GH cell clusters for coordinated responses
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13
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
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14
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

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15
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

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16
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

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17
Q

Fill in the blanks for production of FSH & LH

A

A: Kisspeptin
B: GPR54
C: GnRH

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18
Q

Fill in the blanks for production of FSH & LH

A

A: Kisspeptin
B: GPR54
C: GnRH

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19
Q
A
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20
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

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21
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

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22
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

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23
Q

Explain AEs of thiazide diuretics? [5]

On the levels of:

[Na, K, Ca2+, glucose, cholesterol]

A

Hypokalaemia: K+excretion is enhanced due to the increase in Na+delivered to the distal tubule / CD, where Na is reabsorped at expense of K+

Hypercalcaemia: Ca2+excretion is decreased via a poorly understood mechanism

Hyponatraemia (particularly in old people)

Hyperglycaemia: inhibits insulin secretion slightly

Hypercholesterolaemia: unknown mech

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24
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

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25
Q

What are the two type of K sparing diuretics? [2]

Name two examples of each xx [4]

A

Epithelial Na Channel antagonists
* Amiloride
* Triamterene

Aldosterone antagonists:
* Spironolactone
* Eplerenone

26
Q

What is a osmotic diuretic and which is the most clinically important? [2]

A

Any osmotically active molecule that is freely filtered in the glomerulus, and is not reabsorbed by the tubules, stopping water reabsorption

Most important clinical osmotic diuretic: Mannitol

27
Q

Thiazide diuretics cause increase excretion of which electrolytes? [2]

A

K+, Na+

28
Q

Loop diuretics cause increase excretion of which electrolytes? [4]

A

K+, Na+, H20, Ca, Mg.

29
Q

What are clinical uses of aldosterone inhibitors? [4]

A

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

30
Q

AEs of aldosterone inhibitors? [3]

A

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

31
Q

Why do aldosterone inhibitors lead to hyperkalaemia?

A

Na not excreted, so K kept

32
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

33
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

34
Q

When should you not use diuretics ! [5] key

A

When hypotensive
When dehydrated
When hypokalaemic (Loop/Thiazide)
When hyperkalaemic (Amiloride, aldosterone antagonists)
Post surgery, with a poor urine output

35
Q

Effects of SGLT2 inhibitors? [5]

  • What is effect on GFR? [1]
  • What is effect on albumin levels? [1]
A

Glycosuria: weight loss, reduction in blood glucose, HbA1c reduced

Uric acid reduced

Natuiresis: fall in BP

Reduced hyperinfiltration: reduced albuininuria

Reversible reduction in GFR

36
Q

What is the role of mesengial cells in the glomerulus? [1]

A

Produce basement membrane of glomerulus

37
Q

The endothelial cells in renal corpsucle are:

continuous
discontinuous
fenestrated

A

The endothelial cells in renal corpsucle are:

continuous
discontinuous
fenestrated

38
Q

Why should albumin not be able to pass through glomerular filtration barrier? [2]

A

podocytes create small space (less than 3.5 nm big)

albumin is negatively charged - is repelled by the negatively charged podocytes (particularly via podocyte protein called nephrin)

39
Q

Explain what the role of podocyte slit diaphragm [1] and its components [2]

Mutation to podocytes leads to which syndrome [1]

A

Part of podocyte foot processes that resists movement of molecules:

made from nephrin and podocins

Nephrin transmembrane protein that has a strong negative charge which repel protein from crossing into the Bowman’s space

Mutations to nephrin and podocins can lead to nephrotic syndrome

40
Q

Which cell types are found in the juxtaglomerular apparatus? [3]

What are their functions? [3]

A

The macula densa
* a collection of specialized epithelial cells of the distal convoluted tubule
* enlarged cells compared to surrounding tubular cells
* Sense sodium chloride concentration in the tubule, which in turn reflects the systemic blood pressure

The juxtaglomerular cells of the afferent arterioles
* Responsible for secreting renin
* Derived from smooth muscles cells of afferent arterioles

The extraglomerular mesangial cells
* Flat, elongated cells located near the macula densa
* Function is currently unclear

41
Q

ATII causes constriction of the

afferent arteriole
efferent arteriole

A

ATII causes constriction of the

afferent arteriole
efferent arteriole

42
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.
43
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
44
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

45
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
46
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
47
Q

Bladder cancer is almost always cancer of which cell type? [1]

What is most common symptom? [1]

Name one common cause [1]

A

Urothelial carcinoma (of the transitional cells)

Blood in urine

1/3 caused by smoking

48
Q

Explain MoA of how obesity causes harm via inflammation?

A

Obesity is state of chronic low-level inflammation in response to excess nutrients

In liver, brain, pancreas and adipose tissue

Immune cells are abundant in adipose tissue and obesity-induced activation of their inflammatory response causes changes in their number and activity = inflammation and dysregulated immune system

Why you get cancers and ID

49
Q

The organs affected by obesity can be broadly grouped into three classes:[]

A

The organs affected by obesity can be broadly grouped into three classes: metabolic, mechanical, and mental

50
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

51
Q

What is the impact of obesity on COVID ptx? [1]

Name 2 proposal for how could cause ^? [2]

A

Obesity increases the risk of worse outcome from COVID-19

Proposed to be a consequence of metabolic impairment of organ functioning, leading to insulin resistance

Central fat accumulation could contribute to the increased risk

52
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

53
Q

The physiological responses to weight loss promote weight gain.

Explain why

A

The physiological responses to weight loss promote weight regain

After losing weight, the body responds with a variety of compensatory mechanisms, including changes in the secretion of hormones from the gut, pancreas, and adipose tissue which results in an increase in hunger and desire to eat

54
Q

How do excess lipids cause intracellular lipotoxicity? [2]

A

Lipotoxicity - lipids and their metabolites create oxidant stress to the endoplasmic reticulum and mitochondria.

55
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

56
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

57
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.

58
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

59
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

60
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

61
Q

/

A

.

MET2 (52 decks)

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