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Metabolism 2 > Before the Exam > Flashcards

Before the Exam Flashcards

1
Q

describe what causes normal gap metabolic acidosis

A
  • this is also called hyercloremic metabolic acidosis
  • this is what happens when bicarbonate decreases but the anion gap remains the same due to the increase in chloride ions
  • this is normally due to gut issues
  • it is seen when there is loss of bicarbonate and reduced excretion of hydrogen ions in the kidney - if the kidneys cannot excrete acids effectively then more bicarbonate is needed to buffer them causing a drop in the bicarbonate
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2
Q

what are the causes of normal gap metabolic acidosis

A
  • severe diarrhea
  • chronic laxative abuse
  • villous adenoma
  • external drainage of pancreatic or biliary secretions (eg fistulas)
  • losses via NG tubes
  • administration of acidifying salts
  • urinary diversions
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3
Q

what do alpha intercalated cells secrete and reabsorb

A

secrete
- these cells secrete acid (via an atypical proton and ATPase and H+/K+ exchanger in the form of hydrogen ions

reasborbs
- bicarbonate (via band 3, a basolateral CL-/HCO3- exchanger

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4
Q

what do beta intercalated cells secrete and reabsorb

A
  • secretes bicarbonate (via pendirin a specialised apical CL-/HCO3-)

reabsorbs
- acid (via a basal H+ ATPase)

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5
Q

what are the acute consequences of acidosis

A

Negative inotropic effects
Confusion
Kussmaul’s breathing
Hyperkalaemia

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6
Q

What are the chronic consequences of acidosis

A

Bone reabsorption leading to increased calciuria and this leading to stones

Insulin resistance

Progressive renal impairment

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7
Q

what do growth hormones do in

  • adipose tissue
  • liver
  • skeletal muscles
A

Adipose Tissue:
 Increases lipolysis.
 Reduces glucose uptake.
 Reduces lipogenesis.

Skeletal Muscle:
 Reduces glucose uptake.
 Increases lipoprotein lipase activity.

Liver:
 Increases VLDL secretion.
 Increases production and uptake of HDL and LDLs.

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8
Q

what does GLP-1 do

A
  • inhibits glucagon secretion and hepatic glucose production
  • slows gastric emptying
  • promotes satiety
  • augments glucose-induced inulin secretion
  • rests beta cell function
  • increases insulin biosynthesis
  • promotes B cell differentiation
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9
Q

name some examples of malabsorption procedures

A

e.g. biliopancreatic diversion and Roux-en-Y gastric

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10
Q

name some restrictive procedures

A

adjustable gastric banding,

vertical banded gastroplasty

sleeve gastroplasty

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11
Q

name some expamples of restrictive plus malabsorption procedures

A

duodenal switch,

Roux-en-Y gastric bypass,

intragastric balloon

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12
Q

what is syndromic monogenic obesity

A

Syndromic monogenic obesity is exceptionally rare and characterized by mental retardation, dysmorphic features and organ specific abnormalities, in addition to obesity

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13
Q

what are the intrinsic and extrinsic factors of obesity that can lead to insulin resistance

A

Intrinsic factors as obesity can increase these
- (mitochondrial dysfunction, oxidative stress, ER stress) – this eventually impairs the reaction of the insulin

Extrinsic

  • Accumulation of lipids and their metabolites or increased concentrations of circulating free fatty acids
  • Chronic inflammation
  • Altered adipokine levels
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14
Q

how can pro-inflammatory cytokines, saturated free fatty acids and amino acids cause insulin resistant

A

Pro-inflammatory cytokines, saturated FFAs, amino acids can activate Serine/Threonine kinases that can phosphorylate IRS, reducing its Tyr phosphorylation and also increasing its degradation

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15
Q

Why do not all insulin resistance people have diabetes

A
  • this is because insulin resistance can be overcome by increasing insulin secretion therefore glucose control can be maintained

this happens by

  • new Beta cells being generated in response to insulin resistance associated with obesity or pregnancy
  • islet of langerhans increase in size and number due to beta cell increase in size and number
  • there is an increased beta cell function
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16
Q

what do alpha glucosidase inhibitors do and what are teh side effects

A

 Block disaccharide breakdown.
 Reduces intestinal glucose absorption.
 Decreases postprandial hyperglycaemia.

  • Diarrhoea.
  • Flatulence.
  • Abdominal pain.
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17
Q

what is the clinical presentation of diabetic nephorpathy

A

 Clinical presentation:

  • Hypertension.
  • Proteinuria.
  • Decreased renal function.
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18
Q

what are the symptoms of McCunae-albright syndrome

A

hyper-functioning endocrine organs (goitre),

  • precocious puberty
  • hyperthyroid gotire
  • adrenal hyperplasia
  • somatotroph hyperplasia

bone deformities

Café-
au-lait skin pigmentation.

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19
Q

What is the transcription factor PUOF1 responsive for

A
  • development of TSH, GH, PRL
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20
Q

What receptors do PYY act on

A

Y1-5 receptors expressed peripheral/vagal/central

Y2 is specifically reported as primary receptor mediating effects

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21
Q

what can decrease ghrelin levels in the plasma

A

oxytonmodulin

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22
Q

what does deficiets in the anorexigenic pathway lead to

A

Defects lead to Hyperphagia and obesity.

Genetic deletion of MC4R in both humans and mice has been linked to severe,
hyperphagic obesity.

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23
Q

What adult structures does the ureteric bud develop into

A
  • ureter
  • renal pelvis
  • major and minor calyces
  • collecting tubules
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24
Q

what adult structures does the metanephric (blastema) bud develop into

A
  • Renal glomerulus and capillaries
  • Bowman’s capsule
  • Proximal convoluted tubule
  • Loop of Henle
  • Distal convoluted tubule
25
Q

What are the names of the two symptoms of hypoglycameia

A
  • neuroglycopaenia

- sympathetic response

26
Q

what are the neuroglycopaenia symptoms of hypoglycaemia

A

Dizziness, visual disturbance, hunger
Confusion, personality change, aggression, goes quiet
Coma

27
Q

what is the sympathetic response symptoms of hypoglycaemia

A

sweat
tremors
pallor
nausea

28
Q

What is metabolic syndrome

A
  • A syndrome including an increased risk of cardiovascular disease consisting of:-
  • Insulin resistance/ Type II diabetes
  • Abdominal obesity
  • Dyslipidaemia (particularly hypertriglyceridaemia)
  • Hypertension
29
Q

How does the metabolic syndrome work

A

cells take up fatty aids

  • lipoproteins takes the fatty acids of blood lipids
  • CD36 then carries the fatty acids into the cells
  • these fatty acids are normally metabolised in the mitochondria
  • but if there are too much fatty acid production this can make toxic byproducts such as ceramide
  • the toxic by products block signalling from the insulin receptor
  • this means that the cells cannot take up glucose from the GLUT4 transporter as it cannot go to the surface
30
Q

where and when can you palate the kidneys

A

You can palpate them at the Renal Angle: Junction of 12th rib and lat border of erector spinae muscles
◦ In order to palate as them to inspirited this lowers the diaphragm and moves them down this allows you to palpate them

31
Q

why would Morrisons pouch (hepatorenal recess) be filled with fluid

A

heamoperitoneum,

  • ascites,
  • pancreatitis
32
Q

describe the renal artereis

A
  • These split form segmental arteries
  • Interlobar arteries
  • Arcuate arteries
  • Interlobular arteries in the cortex
  • Will then go into the nephron area – afferent arteriole, glomuerlus, efferent arteriole, peritiubular capillaeis/vasa recta,
33
Q

name the nerve supply that make up the renal plexus

A
  • Sympathetic T10-L2
  • thoracic and lumbar splanchics
  • parasympathetic vagus
  • visceral afferent fibres T10-L2
34
Q

what cells secrete what in the medulla

A

.- 80% of the medulla cells secrete adrenaline

  • 20% noradrenaline,
  • a few dopaminergic cells
35
Q

How does the renal system acts on aldosterone

A
  • via the principal cell

- via the intercalated cell

36
Q

What are principal cells

A

Principal cells are the main Na+ reabsorbing cells and the site of action of aldosterone, K+-sparing diuretics, and spironolactone.

37
Q

How do you diagnose conns syndrome

A

Aldosterone:Renin Ratio
- measure the aldostoenre and renin ratio, if renin levels are 0 and aldosterone is high then conns syndrome

Saline suppression test
- the low fluid volume increases aldosterone production therefore if you give them a bag of saline which raises the fluid level and there aldosterone levels are still high then this is pathological

CT Adrenal

Adrenal venous sampling
- this is when you insert a catheter into the groin and measure the aldosterone level form each adrenal gland

Metomidate PET

38
Q

How do you diagnose Cushing syndrome

A

Overnight dexamethasone suppression test
– give tablet of dexamethasone at bedtime and measure the next morning they should be 0 or less than 20 nano meteres, if there not then there is a cortisol problem

24 hour urine free cortisol

LDDST: 0.5mg dexamethasone every 6 hours for 48 hours

Cortisol day curve plus midnight sleeping cortisol – measures cortisol throughout the day, if you have cushings disease the levels of cortisol will stay up all long

Blood test – midnight should be low

39
Q

What can differitate between a pituitary adenoma and a ectopic ACTH secreting tumour as the cause of Cushings syndrome

A
  • Inferior petrosal sinus sampling distinguishes between a pituitary adenoma and an ectopic ACTH secreting tumour as the cause of Cushing’s syndrome
  • Blood is drawn directly from the venous sinuses around the pituitary.
    High ACTH in the petrosal veins in a patient with confirmed Cushing’s compared to the periphery =
    Pituitary Source of ACTH

ACTH in the petrosal veins equal to the periphery with confirmed Cushing’s = Peripheral source of ACTH

40
Q

How do you diagnose Addison disease

A

Low 9am cortisol
High ACTH
Short Synacthen Test – synthetic ACTH – if adrenal glands are working expect to increase the amount of cortisol that is being produced

41
Q

what are the two types of tumours from chromaffin cells

A

phaeochromocytoma

paraganglioma

42
Q

how do you make a diagnosis of PPGL

A 
•	24 hour urine metanephrines
•	Plasma metanephrines
•	CT/MRI adrenals and abdomen
•	123I-MIBG scintigraphy
- MIBG – tracer taken up ny neuroendocrine cells and localise din the granules where they caetcholamines are made
43
Q

What is the treatments of PPGL

A

• Surgical resection
• Pre-operative alpha and beta-blockade – because the symptoms of these tumours are due to too much alpha and beta cell stimulus, can lead to anaesthetic bad reaction without these
– Phenoxybenzamine 10mg bd and titrate
– Propranolol 10mg qds and titrate
• Acute crisis: IV phentolamine or nicardipine
• Avoid opiates – adrenal cells have opiate receptors on them
• 131I-MIBG therapy for malignant disease

44
Q

describe the embryo development of the thyroid

A
  • develops over 24 days
  • made from 2 pharyngeal pouches and 1 groove, more over following days
  • then we develop additional grooves and pouches over the following days.
  • Pouch 3 - inferior parathyroid and thymus
  • Pouch 4 - superior parathyroid and ultimobranchial body
    Ultimobranchial body - C-cells
  • Thyroid diverticulum starts at foramen cecum and descends Non duct closure - thyroglossal cyst
45
Q

what inhibits TBG binding

A

Binding inhibited by phenytoin, salicylate, furosemide

46
Q

what are the transports that regulate thyroid hormone uptake

A

MCT8
MCT10
OATP1C1

47
Q

how do you treat hyperthyroidism

A

Thionamide drugs

  • Propylthiouracil
  • Carbimazole

Radioactive Iodine I-131

Thyroidectomy

48
Q

name the three things that the globular filtration barrier is made out of

A
  1. Fenestrated capillary endothelium
  2. Basement membrane
  3. Podocyte layer of Bowman’s capsule – end feet that stick down on the basement membrane, between the podocyte process they have membranes and proteins that can regulate and charge
49
Q

what epithelium is int he collecting ducts

A

columnar

- everywhere else in the renal tubular has cuboidal epithelium

50
Q

define the glomerular filtration rate

A
  • this is the total amount of fluid filtered through all the glomeruli in both kidneys
  • usually 120-125 ml/min
51
Q

what is clearance

A

it is the effective volume of plasma completely cleared of a substance per minute

52
Q

what happens if there is a defect with the apical Na/Cl/K in the thick ascending loop

A

• Bartter’s type 1
mimic of the effects of furosemide.

causes

  • Hypokalaemia,
  • metabolic alkalosis,
  • hypocalcaemia,
  • hypomagnasaemia
53
Q

what happens if there is a defect in the apical sodium chloride con transporter in the distal tubule

A

• Gitelman’s:
- Mimic of thiazide use.

causes

  • Hypokalaemia,
  • metabolic alkalosis,
  • hypomagnasaemia,
  • hypercalcaemia
54
Q

what are the types of lower urinary tract symptoms

A
  • Storage irritative symptoms – frequency, nocutria, urgency, urgency incontinence
  • Voiding (obstructive) symptoms – hesitancy, straining, poor flow, intermittency, incomplete emptying – also terminal dribbling, dysuria, haematuria (blood in urine)
  • Overactive bladder (to do with storage symptoms)– urgency with or without incontinence usually with frequency and nocutira
55
Q

what factors make up the international prostate symptom score

A
  • incomplete emptying
  • frequency
  • incontinency
  • urgency
  • weak stream
  • straining
  • nocturia
56
Q

name some disorders of

  • anatomical
  • functional
  • medical
A
  • Anatomical disorders – obstructive, incontinence
  • Functional disorders – stroke, spinal cord injury, neurologic disease, idiopathy
  • Medical disorders – cardiac, hepatic and renal failure
57
Q 
name some 
- storage 
- voiding 
- both or neither 
symptoms
A

storage

  • incomplete emptying
  • frequency
  • urgency

voiding

  • intermittency
  • weak stream
  • straining

both or niether
- nocturia

58
Q

Which of the following are released in response to food intake and is proportional to calorie intake?

A

pancreatic polypeptide

59
Q

hyperkalemia is associated with …

A

DKA

Metabolism 2 (40 decks)

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