Yr 2 EOYS ^2 > MET EOYS3 > Flashcards

MET EOYS3 Flashcards

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1
Q

PYY has the biggest effect on which part of the GI system

Stomach
Duodenum
Jejunum
Ileum
Colon

A

PYY has the biggest effect on which part of the GI system

Stomach
Duodenum
Jejunum
Ileum
Colon

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2
Q

PYY has the is produced from which type of cells:

D cells
A cells
L cells
B cells

A

PYY has the is produced from which type of cells:

D cells
A cells
L cells
B cells

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3
Q

Thiolactone is produced due to a deficiency in which two molecules [2]

What does increased thiolactone levels lead to? [1]

A

B12 & Folate Deficiency

Leads to atherosclerosis

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4
Q

Impaired genetic compensation: genetic component

How do most of the genes associated with DMT2 influence insulin [2]

A

impairing insulin secretion rather than insulin action

Gene risk variants are to do with the regulators of β cell turnover or regeneration

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5
Q

Impaired genetic comepensation: environmental component

Which envrionmental factors within body influence DMT2 infuence? [4]

A

Increased circulating FFAs (lipotoxicity)

Hyperglycaemia (glucotoxicity)

Combination of the two (glucolipotoxicity)

Hyperinsulinemia

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6
Q

What is Monogenic diabetes? [1]

Specifically how is it caused / insulin affected? [2]

A

Caused by a mutation in a single gene (one of over 40 genes): Means theres 40 types of MODY

Most cases are Maturity Onset Diabetes of the Young (MODY)

Caused by:
* prevent the insulin sensing glucose metabolism in B-cells

  • Due to: impairment of insulin secretion/pancreatic βcell dysfunction
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7
Q

What is LADA?

What are characteristics of LADA? [2]

A

Latent Autoimmune Diabetes of Adults (LADA): Features of both Type 1 and Type 2 (type 1.5)

Immunologically similar to T1 - produce DMT1 antibodies but destruction is slower than in T1.

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8
Q

What HbA1c is used as cut off for diabetes? [1]

A

An HbA1c of 48 mmol/mol (6.5%) is recommended as the cut point for diagnosing diabetes

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9
Q

Which treatments for DMT2

inhibitGNG [1]
increase insulin sensistivity [2]
stimulate insulin secretion [2]

two others? [2] ?

A

Inhibits GNG:
* Metformin: inhibits GNG at liver

Increases insulin sensitivity:
* Metformin
* Thiazolidinediones: Enhance GLUT4 uptake into the cell membranes (in adipocytes - so causes weight gain) via PPAR-y gene

Stimulation of insulin secretion:
* Sulfonylureas: close ATP sensitive K chance which regulates insulin secretion
* Prandial glucose regulators: same as above but faster

Others:
* GL1-P receptor agonists
* DPP-4 inhibitors: DPP-4 inhibits GL1-P

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10
Q

How does DKA occur?

A

In the absence of insulin there is an unrestrained increase in hepatic gluconeogenesis and peripheral glucose uptake by tissues such as muscle is reduced

High circulating glucose levels result in an osmotic diuresis (since increased glucose in urine which pull more water into urine) by the kidneys and consequent dehydration and loss of electrolytes

Peripheral lipolysis occurs leading to an increase in circulating free fatty acids (FFAs) which are then broken down to acetyl-coenzyme A (CoA), but little oxaloacetate within the liver cells and this, in turn, is converted to ketone bodies within the mitochondria. (no Kreb’s cycle)

Ketone bodies are in excess

Ketone bodies dissociate: H+

Causes metabolic acidosis w/ raised anion gap.

Vomiting leads to further electrolye loss

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11
Q

What is difference between non-proliferative and proliferative retinopathy?

A

Both occur because of damage to BV in back of eye

Non-profilerative: ‘Cotton wool’ dilation of retina veins causes internal haem. oedema causes vision loss

Proliferative: New BV proliferate near optic disc and bleed: detachment of retina

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12
Q

MoA of diabetic nephropathy?

A

PKA activation -> collagen/fibronectin proliferation -> capillary occlusion -> thickening of glomerular basement membrane. PKA activation -> increase in NADPH -> ROS

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13
Q

MoA of diabetic retinopathy?

A

Hyperglycaemia -> increased PKA activity -> reduced retinal blood flow due to vasoconstriction
PKA activity -> vascular permeability angiogenesis -> macular oedema

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14
Q

Which of the following drug treatments for diabetes causes weight gain? [2]

  • Sulfonylureas - e.g. gliclazide, glibenclamide and tolbutamide
  • Metformin
  • SGLT2 Inhibitors
  • Thiazolidinediones e.g Pioglitazone or Rosiglitazone
A

Which of the following drug treatments for diabetes causes weight gain? [2]

  • Sulfonylureas - e.g. gliclazide, glibenclamide and tolbutamide
  • Metformin
  • SGLT2 Inhibitors
  • Thiazolidinediones e.g Pioglitazone or Rosiglitazone
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15
Q

Under normal B12 and Folate levels what is homocysteine converted to? [1]

Deficient B12 and Folate levels what is homocysteine converted to? [1]
What pathology does this lead to? [1]

A

When the body has Folate and vit B12 (necessary co factors for)
* methionine synthase enzyme: converts homocysteine –> methionine.

BUT: without Folate and B12:
* homocysteine -> homocysteine thiolactone (damages endothelium
= ATHEROSCLEROSIS

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16
Q

Chronic deficiency in folate causes low [] and high blood [] levels

A

Chronic deficiency in folate causes low methionine and high blood homocysteine levels

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17
Q

When chronic folate deficiency: homocysteine is converted to toxic [] which damages endothelium.

A

When chronic folate deficiency: homocysteine is converted to toxic thiolactone which damages endothelium.

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18
Q

What is metabolic syndrome a combination of? [4]

A

Syndrome of increased CVD risk because of:

  • Insulin resistance/ Type II diabetes
  • Abdominal obesity
  • Dyslipidaemia (particularly hypertriglyceridaemia)
  • Hypertension

These factors cluster together more frequently than expected by chance !

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19
Q

Role of the following of on firing of ECC vesicles?

5HT [1]
Leptin [1]
Ghrelin [1]

A

5HT - increases firing
Leptin - decreases firing
Ghrelin - decreases firing

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20
Q

Which cells release PYY? [1]
Where is PYY predominately found? [1]
What effect does PYY have on NPY [1] and POMC neurones [1]

A

Which cells release PYY? [1]: L cells in GI tract
Where is PYY predominately found: Colon –> rectum
What effect does PYY have on NPY: inhibits
and POMC neurones: activates

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21
Q

AGRP/NPY neurones in arcuate nucleus of hypothalamus are activated by which hormone? [1]

What biochem effect does this have? [1]

A

AGRP/NPY neurones in arcuate nucleus of hypothalamus are activated by which hormone? [1]
Ghrelin

What biochem effect does this have? [1]
Causes a release of Y1 receptors

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22
Q

Label A-E xx

A

A: GLP-1
B: PYY
C: Ghrelin
D: Leptin
E: Insulin

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23
Q

Role of malonyl-coA? [1]

[] malonyl-coA supresses food intake
[] malonyl coA increases food intake

A

Malonyl-CoA is the substrate for fatty acid synthase, but it is a key determinant for the entry of fatty acids into the mitochondria, and appears to play a pivotal signaling role in appetite regulation.

Increased malonyl-coA supresses food intake
Decreased malonyl coA increases food intake

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24
Q

Explain how overall food intake decreases in response to increased energy levels? [1]

Explain how ^ occurs [3]

Study These Flashcards
A

Increased M-CoA - stimulates FA synthesis –» therefore suppresses appetite

More ATP over AMP -> increased denovo FA synthesis -> increased M-CoA -> stimulation of POMC/CART + suppression NYP/AgRP -> decreased food intake

25
Effect of serotonin on appetite? Effect on POMC and AgRP neurones?
Serotonin (5HT): **anorexigenic**: augmentation of brain 5HT **inhibits food intake**, depletion promotes weight gain They **increase signalling** (simulate) activity in the **POMC** neurones (via the 5HT2CR) They **decrease** signalling in the **AgRP** neurones (via the 5HT1BR)
26
Which of the following are released from the stomach: A: GLP-1 B: PYY C: Ghrelin D: Leptin E: Insulin
Which of the following are released from the stomach: A: GLP-1 B: PYY **C: Ghrelin** D: Leptin E: Insulin
27
Which of the following is the action of PYY? Inhibits excitatory appetite neurones Stimulates excitatory appetite neurones Inhibits inhibitory appetite neurones None of the above
Which of the following is the action of PYY? **Inhibits excitatory appetite neurones** Stimulates excitatory appetite neurones Inhibits inhibitory appetite neurones None of the above
28
Alpha-MSH and Beta-endorphin may be produced from which neurotransmitter? CART (cocaine- and amphetamine regulated transcript) POMC (pro-opiomelanocortin) NPY (Neuropeptide Y) AgRP (Agouri-related peptide)
Alpha-MSH and Beta-endorphin may be produced from which neurotransmitter? CART (cocaine- and amphetamine regulated transcript) **POMC (pro-opiomelanocortin)** POMC can be cleaved into other neurotransmitters such as alpha-MSH and beta-endorphin. **These also act to suppress hunger**. NPY (Neuropeptide Y) AgRP (Agouri-related peptide)
29
Which vertebral layers does the thyroid cartilage sit between C3-T2 C4-T2 C5-T2 C4-T1 C5-T1
Which vertebral layers does the thyroid cartilage sit between C3-T2 C4-T2 C5-T2 C4-T1 **C5-T1**
30
Which two structures are closely related anatomically External larnyngeal nerve and inferior thyroid artery External larnyngeal nerve and superior thyroid artery Internal larnyngeal nerve and inferior thyroid artery Internal larnyngeal nerve and superior thyroid artery
Which two structures are closely related anatomically External larnyngeal nerve and inferior thyroid artery **External larnyngeal nerve and superior thyroid artery** Internal larnyngeal nerve and inferior thyroid artery Internal larnyngeal nerve and superior thyroid artery
31
Inferior vein drainage from the thyroid goes into which of the folloiwng External jugular vein Internal jugular vein Brachiocephalic vein Subclavian vein Thyrocervical trunk
Inferior vein drainage from the thyroid goes into which of the folloiwng External jugular vein Internal jugular vein **Brachiocephalic vein** Subclavian vein Thyrocervical trunk
32
Which pathways are activated during hyperglycaemia that can cause damage [3]
1. Oxidative stress: get increased expression and activity of vascular NADH oxidase. **Leads to ROS accumulation** 2. Increase in **polyol pathway**: increased **AGE production** 3. Converted to **PKC pathway**: creates more ROS
33
What are AGE products?
**Advanced Glycation End products** (AGEs) are proteins or lipids that become glycated Causes: **Structural modificaiton of proteins:** basement membrane thickness, reduced vascular elasticity etc **Interaction with AGE receptors:** activation of signalling, gene expression, secretion of pro-inflammatory molecules, increased production of free radicals etc)
34
Describe the arterial supply to the thyroid [2] And their sources [2]
* The **superior thyroid artery** (STA) arising from the **external carotid artery** (ECA) * The **inferior thyroid artery** (ITA) branching from the **thyrocervical trunk**
35
Describe venous drainage & route of the thyroid [5]
The thyroid gland is drained via the **superior, middle, and inferior thyroid veins**: form a **venous plexus around the thyroid gland.** [3] Superior and middle veins drain into the **internal jugular vein** [1] Inferior vein: empties into the **brachiocephalic vein** [1]
36
What supplies sympathetic [1] & parasympathetic [1] nervous supply to thryoid?
SNS: **Cervical ganglion** PNS: **Recurrent LN**
37
Describe the blood supply to the adrenal glands? [3] & sources? [3]
The adrenal glands have a rich blood supply via three main arteries: Superior adrenal artery – arises from the inferior phrenic artery Middle adrenal artery – arises from the abdominal aorta. Inferior adrenal artery – arises from the renal arteries.
38
Describe adrenal venous drainage [2]
Right and left adrenal veins drain the glands. The **right adrenal vein** drains into the **inferior vena cava** The **left adrenal vein** drains into the **left renal vein**.
39
Label A-E
A: Internal branch of **superior laryngeal nerve** B: **Inferior thyroid artery** C: **Superior laryngeal nerve** D: **Glossopharyngeal nerve** E: Inferior laryngeal branch of **recurrent laryngeal nerve**
40
Label 40-45
40 Internal carotid artery 41 External carotid artery 42 Superior laryngeal artery 43 Superior thyroid artery 44 Common carotid artery 45 Thyroid ansa of sympathetic trunk and inferior thyroid artery
41
A 65-year-old man is due to undergo a radical prostatectomy for carcinoma of the prostate gland. To which of the following lymph nodes will the tumour drain primarily? Internal iliac Para-aortic Meso rectal Superficial inguinal None of the above
A 65-year-old man is due to undergo a radical prostatectomy for carcinoma of the prostate gland. To which of the following lymph nodes will the tumour drain primarily? **Internal iliac** Para-aortic Meso rectal Superficial inguinal None of the above
42
A 47-year-old man presents with episodes of a racing heartbeat that occur 4 to 6 times daily and are associated with sweating and facial flushing. In between episodes, he is asymptomatic. Assuming a tumor is the cause of these symptoms, how does the tumor affect blood glucose regulation? A. Decrease serum glucose and increase insulin secretion B. Increase serum glucose only C. Decrease serum glucose only D. Increase serum glucose and decrease insulin secretion
**D. Increase serum glucose and decrease insulin secretion** **Pheochromocytoma** is a tumor of the adrenal medulla that causes excess catecholamine release. Catecholamines increase glucagon secretion via beta-2 receptors and activate glycogenolysis. This results in increased serum glucose.
43
Which of the following causes of Cushing's syndrome does the phrase "Cushing's disease" specifically refer to? Pituitary adenoma Adrenal adenoma Ectopic ACTH production Iatrogenic
Which of the following causes of Cushing's syndrome does the phrase "Cushing's disease" specifically refer to? **Pituitary adenoma** Adrenal adenoma Ectopic ACTH production Iatrogenic
44
Which one of the following statements best describes an Addisonian crisis? Severe adrenal insufficiency resulting in dangerously low serum cortisol levels Dangerously high serum cortisol levels Severe adrenal insufficiency resulting in dangerously low serum testosterone levels Dangerously high levels of testosterone
Which one of the following statements best describes an Addisonian crisis? **Severe adrenal insufficiency resulting in dangerously low serum cortisol levels** Dangerously high serum cortisol levels Severe adrenal insufficiency resulting in dangerously low serum testosterone levels Dangerously high levels of testosterone
45
What is the most common cause for the overproduction of growth hormone in acromegaly? Hypothalamic lesion Pituitary adenoma Pituitary lesion Hyperplasia of the pituitary stalk
What is the most common cause for the overproduction of growth hormone in acromegaly? Hypothalamic lesion **Pituitary adenoma** Pituitary lesion Hyperplasia of the pituitary stalk In around 99% of cases, acromegaly is caused by a pituitary adenoma, specifically overgrowth of the somatotrope cells which are responsible for growth hormone production. In very rare cases acromegaly can be caused by ectopic production of growth hormone by carcinoid tumours.
46
What is Addison's disease? Addison’s disease is a long-term endocrine disorder in which the adrenal glands do not produce enough steroid hormones. Addison's disease involves the overproduction of androgens by the adrenal medulla. Addison's disease involves the underproduction of androgens by the adrenal medulla. Addison's disease involves the overproduction of cortisol and aldosterone by the adrenal cortex.
What is Addison's disease? **Addison’s disease is a long-term endocrine disorder in which the adrenal glands do not produce enough steroid hormones.** Addison's disease involves the overproduction of androgens by the adrenal medulla. Addison's disease involves the underproduction of androgens by the adrenal medulla. Addison's disease involves the overproduction of cortisol and aldosterone by the adrenal cortex.
47
Which enzyme is most commonly deficient in congenital adrenal hyperplasia? [1] Which hormones does this mean are increased? [2]
**21-hydroxylase** 21-hydroxylase needed to produce **cortisol** and **aldosterone**; causes more **androgens** to be made
48
Which enzyme is the final step in cortisol production? 21-hydroxylase 11B-hydroxylase 5a-reductase 17B-HSD
Which enzyme is the final step in cortisol production? 21-hydroxylase **11B-hydroxylase** 5a-reductase 17B-HSD
49
Which enzyme is the final step in testosterone production? 21-hydroxylase 11B-hydroxylase 5a-reductase 17B-HSD
Which enzyme is the final step in testosterone production? 21-hydroxylase 11B-hydroxylase 5a-reductase **17B-HSD**
50
Side-effects include gastrointestinal upset and lactic acidosis: Metformin SGLT-2 Inhibitors GLP-1 agonists Thiazolidinediones
Side-effects include gastrointestinal upset and lactic acidosis (**common in exams)** **Metformin** SGLT-2 Inhibitors GLP-1 agonists Thiazolidinediones
51
Which one of the following actions is directly caused by cortisol? Increases gastric motility Decreases osteoclastic activity Decreases renal reabsorption of phosphate Upregulates alpha1 receptors on arterioles
Which one of the following actions is directly caused by cortisol? Increases gastric motility Decreases osteoclastic activity Decreases renal reabsorption of phosphate **Upregulates alpha1 receptors on arterioles**
52
Thyrotoxicosis is most likely to present with the following blood tests: High TSH; Low T4 Low TSH; Low T4 High TSH; High T4 Low TSH; High T4
Thyrotoxicosis is most likely to present with the following blood tests: High TSH; Low T4 Low TSH; Low T4 High TSH; High T4 **Low TSH; High T4**
53
Explain the difference in primary and secondary hyperaldosteronism
Primary hyperaldosteronism: * excess production of the **adrenal gland** (zona glomerulosa) * can present more commonly as a **primary tumor** in the gland known as **Conn syndrome** or **bilateral adrenal hyperplasia** Secondary hyperaldosteronism: * **Excessive** **activation** of **RAAS** * renin-producing tumor, renal artery stenosis, or edematous disorders like left ventricular heart failure, pregnancy, cor pulmonale, or cirrhosis with ascites.
54
Catecholamines monoamines (Dopamine, norepinephrine, and epinephrine) are synthesised from which two molecules? [2] Where? [1]
Adrenaline synthesised from **Phenylalanine** and **Tyrosine** At: **chromaffin** cells of the **adrenal medulla**
55
Effect of cortisol in: a) the liver [2] b) the muscle [2] c) adipocytes [2]
(opposite of insulin; similar to glucagon) In the liver: * **enhances gluconeogenesis** * **inhibits glycogen synthesis** In muscle: * **inhibits glucose uptake/utilisation** * **stimulates protein degradation** In adipocytes: * it stimulates **lipolysis** * **Rapid mobilisation of glucogenic amino acids and glycerol/fatty acids from cellular stores**
56
Growth hormone is stimulated by the release of which hormone? [1] Growth hormone is inhibited by the release of which hormone? [1]
Growth hormone: - stimulated by **growth hormone-releasing hormone** (**GHRH**) - inhibited by **somatostatin** (**SSTN**)  
57
What are the metabolic effects of growth hormone at: a) liver [2] b) sk. muscle c) adipose tissue
What are the metabolic effects of growth hormone at: a) adipose tissue: * **reduces lipogenesis** * **Increases lipolysis** * Overall effect: reduces body fat mass b) sk. muscle * **Reduces glucose uptake** * **Increases b oxidation** c) liver: * **increases production and uptake of IDL, LDL and HDL**
58
What is the effect of growth hormone on IGF-1? What is the effect of IGF-1 activated on renal GNG [1] and glucose transport? [1]
IGF1 = Insulin-like growth factor 1 GH is a regulator of IGF1, specifically it **decreases renal GNG** and **increases glucose transport**
Yr 2 EOYS ^2
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