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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
What are the two type of K sparing diuretics? [2] Name two examples of each xx [4]
**Epithelial Na Channel antagonists** * Amiloride * Triamterene **Aldosterone antagonists:** * Spironolactone * Eplerenone
26
What is a osmotic diuretic and which is the most clinically important? [2]
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
Thiazide diuretics cause increase excretion of which electrolytes? [2]
K+, Na+
28
Loop diuretics cause increase excretion of which electrolytes? [4]
K+, Na+, H20, Ca, Mg.
29
What are clinical uses of aldosterone inhibitors? [4]
Hyperaldosteronism (Conns) Heart failure Hypokalaemia (from other diuretics) Cirrhosis
30
AEs of aldosterone inhibitors? [3]
**Hyperkalaemia** **Hyperkalaemia** --> can lead to cardiac arrythmias and death **Hyperkalaemia** Gynecomastia (not eplerenone) Hyponatraemia (Cirrhosis)
31
Why do aldosterone inhibitors lead to hyperkalaemia?
Na not excreted, so K kept
32
When would you use osmotic diuretic clinically? [1]
**Clinical use:** * Cerebral odema AEs: * Transient fluid overload: **pulmonary odema** * If using glucose: **DKA/HHS** * If using urea: **Disequilibrium syndrome**
33
Explain MoA of SGLT-2 inhibitors
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
When should you not use diuretics ! [5] key
When **hypotensive** When **dehydrated** When **hypokalaemic** (Loop/Thiazide) When **hyperkalaemic** (Amiloride, aldosterone antagonists) **Post surgery**, with a poor **urine output**
35
Effects of SGLT2 inhibitors? [5] - What is effect on GFR? [1] - What is effect on albumin levels? [1]
**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
What is the role of mesengial cells in the glomerulus? [1]
Produce basement membrane of glomerulus
37
The endothelial cells in renal corpsucle are: continuous discontinuous fenestrated
The endothelial cells in renal corpsucle are: continuous discontinuous **fenestrated**
38
Why should albumin not be able to pass through glomerular filtration barrier? [2]
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
Explain what the role of podocyte slit diaphragm [1] and its components [2] Mutation to podocytes leads to which syndrome [1]
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
Which cell types are found in the juxtaglomerular apparatus? [3] What are their functions? [3]
**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
ATII causes constriction of the afferent arteriole efferent arteriole
ATII causes constriction of the afferent arteriole **efferent arteriole**
42
How can you distinguish that cells are from the CD?
- 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
Describe the different layers of the ureter [3]
- an **inner longitudinal** layer **smooth muscle** - an **outer circular** layer of **smooth muscle** - **lumen** of the ureter is covered by **transitional epithelium**
44
Describe pathophysiology of minimal change disease
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
Describe pathophysiology of diabetic nephropathy
- 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
Describe pathophysiology of primary Glomerulonephritis - What is it caused by? [2] - What happens to structure of glomerulus? [3]
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
Bladder cancer is almost always cancer of which cell type? [1] What is most common symptom? [1] Name one common cause [1]
Urothelial carcinoma (of the transitional cells) Blood in urine 1/3 caused by smoking
48
Explain MoA of how obesity causes harm via inflammation?
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
The organs affected by obesity can be broadly grouped into three classes:[]
The organs affected by obesity can be broadly grouped into three classes: **metabolic**, **mechanical**, and **mental**
50
Obesity and comorbidities: Name 4 impacts of immunity because of obesity
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
What is the impact of obesity on COVID ptx? [1] Name 2 proposal for how could cause ^? [2]
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
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.
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 f**urther increased health risks**
53
The physiological responses to weight loss promote weight gain. Explain why
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
How do excess lipids cause intracellular lipotoxicity? [2]
Lipotoxicity - lipids and their metabolites create **oxidant stress** to the **endoplasmic** **reticulum** and **mitochondria**.
55
Which pathology is depicted using immunohistocomplex staining? IgA nephropathy Membranous change disease DIabetic nephropathy Glomerulosclerosis
Which pathology is depicted using immunohistocomplex staining? **IgA nephropathy** Membranous change disease DIabetic nephropathy Glomerulosclerosis
56
Which pathology is depicted using immunohistocomplex staining? IgA nephropathy Membranous change disease DIabetic nephropathy Glomerulosclerosis
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
Which pathology is depicted in this histology slide? IgA nephropathy Membranous change disease DIabetic nephropathy Glomerulosclerosis
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
Which pathology is depicted in this histology slide? IgA nephropathy Membranous change disease DIabetic nephropathy Glomerulosclerosis
Which pathology is depicted using immunohistocomplex staining? IgA nephropathy Membranous change disease **DIabetic nephropathy** - note the Kimmelstiel-Wilson nodules Glomerulosclerosis
59
Which pathology is depicted in this histology slide ? IgA nephropathy Membranous change disease DIabetic nephropathy Glomerulosclerosis
Which pathology is depicted using immunohistocomplex staining? **IgA nephropathy - mesengial hypercellulairty** Membranous change disease DIabetic nephropathy Glomerulosclerosis
60
Which pathology is depicted using slide? IgA nephropathy Membranous change disease DIabetic nephropathy Glomerulosclerosis
Which pathology is depicted using immunohistocomplex staining? IgA nephropathy **Membranous change disease** DIabetic nephropathy Glomerulosclerosis
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MET2 (52 decks)

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