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Phase 3B: Gastroenterology > Basic science > Flashcards

Basic science Flashcards

1
Q

What is the hormone that regulates systemic iron homeostasis

A

hepcidin

  • downregulates cellular iron exporter - ferroportin - found in enterocytes, hepatocytes, macrophages
  • enterocytes sequester iron until they are lost by desquamation
  • Low ferroportin also prevents release of iron stores from RESlo

Low hepcidin ⇒ decreases absorption of dietary iron and decreases the flow of stored iron and recycled iron into plasma

Upregulated in:

  • Iron excess
  • Inflammation

Downregulated in:

  • hypoxia
  • erythropoiesis
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2
Q

What is transferrin? How do you interpret it?

A

Iron transport protein

    • total iron binding capacity is an indirection measure of transferrin levels
  • High transferrin - iron deficiency, pregnancy, exogenous oestrogen
  • Low transferrin - inflammation, chronic liver disease, malnutrition
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3
Q

How do you interpret serum iron?

A

Affected by diurnal variation, recent iron intake and acute phase responses

Limited utility in assessment of overall iron status, instead, used to calculate transferrin saturation

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4
Q

What is ferritin

A

Storage protein that binds iron

Synthesised in:

  • bone marrow
  • liver

Increased in:

  • inflammation
  • liver disease
  • malignancy
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5
Q

What is the transferrin saturation

A

% of transferrin’s carrying capacity that is saturated with iron

Decreased saturation is suggestive of

  • iron deficiency OR
  • Inflammation
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6
Q

What are the functions of magnesium

A

Second most abundant cation

Functions:

  • Co-factor for DNA & Protein synthesis & Oxidative Phosphorylation
  • Enzyme co-factors: ATPases, kinases, ion transporters
  • Neuromuscular excitability - Ca2+ channel antagonist
  • PTH secretion and function
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7
Q

What is the requirment of magnesium per day? Where is dietary magnesium found? Where is it absorbed? How is it excreted?

A

300mg

Sources:

  • Cereals
  • green vegetables
  • Beans
  • Nuts

Absorption

  • Active/saturable
  • Passive/non-saturable

80% filtered in glomeruli

  • nearly all reabsorbed - most in LoH
  • Reabsorption can be varied from 0 - 99%, depending on plasma Mg2+
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8
Q

What are some reasons for hypomagnesaemia

A

Decreased intake

  • Alcoholism
  • IV fluids or TPN

Increased losses

  • GI tract: Diarrhoea, malabsorption, fistula
  • Renal tubular disorders
  • Drugs: Diuretics, aminoglycosides, cisplatin, PPI
  • Hypercalcaemia

Redistribution

  • Acute pancreatitis
  • Hungry bones - after correction of long-standing primary hyperparathyroidism
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9
Q

What are the clinical effects of hypomagnesaemia

A

Neuromuscular

  • Same as for calcium e.g. weakness, paraesthesia…

Cardiovascular

  • ECG abnormalities
  • Arrhythmias

Metabolic

  • Hypokalaemia due to renal loss of K+ –> swap Mg2+ for K+ in urine
  • Hypocalcaemia due to low PTH and resistance

NB) if you have hypokalaemia due to low magnesium, must correct magnesium in order to increase plasma K+

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10
Q

How do you correct hypomagnesaemia

A

Mild to moderate

  • oral replacement w/ magnaspartate

Moderate w/ symptoms or severe

  • IV Mg, then oral replacement

NB) intracellular ions require a lot of replacement. After restoring plasma level, intracellular stores must be replenished

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11
Q

What might cause hypermagnesaemia

A

Uncommon as requires very high intake plus renal impairment or IV Mg

NB) high dose Mg used to treat pre-eclampsia/eclamptic fits

Neurology

  • loss of deep tendon reflexes
  • Flaccid paralysis
  • Mental changes

Cardiovascular

  • bradycardia
  • Hypotension
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12
Q

What is phosphate used for?

A

Intracellular

  • Structural: Lipids, proteins
  • High energy phosphate bonds: ATP
  • Nucleic acids: DNA, RNA
  • Signalling: cAMP

Extracellular

  • Present as HPO4-, H2PO4-
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13
Q

How is phosphate level regulated?

A

90% filtered by glomerulus

Mostly reabosrbed by Proximal tubule - energy dependent

Regulated by

  • PTH
  • Active vit D
  • FGF23
    • Glycoprotein produced by bone cells
    • Reduces renal reabsorption to lower serum PO4-
    • Inhibits activation of Vit D
    • Increased by:
      • Genetic disorders
      • Tumour secretion
      • Drugs

Plasma phosphate affected by:

  • Insulin
  • GH
  • Glucocorticoids
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14
Q

What are some mechanisms of hypophosphataemia?

A

Inadequate intake - chronic

Transcellular shift - acute

  • insulin
  • respiratory alkalosis
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15
Q

Who is at risk of refeeding syndrome? How do you avoid it?

A

Malnourished

  • cancer/cachexia
  • eating disorders
  • alcoholism
  • post surgery

Avoid by:

  • Anticipating it
  • Checking and replacing K+, Mg2+, PO4- before starting TPN
  • Nutrition MDT

Insulin spike drives K+, Mg2+, PO4- into cells, with glucose. This causes dangerous low levels

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16
Q

What are other causes of hypophosphataemia

A

Drugs

  • Salicylates
  • Sympathomimetics/beta-adrenergics
  • Parcetoml OD
  • Iron infusions

Renal loss

  • Proximal tubule damage
  • fanconi syndrome

FGF23 secretion

17
Q

How does hypophosphataemia present

A

Multisystem

  • Anaemia, WBC function, platelets
  • Muscle weakness, rhabdomyolysis, respiratory failure
  • CNS: Confusion, seizures, coma
  • CVS: cardiomyopathy
  • Bones: pain, osteomalacis

Can be moderate and self limiting without clinical effects

18
Q

What are the mechanisms for hyperphosphataemia

A

Increased intake

  • Phosphate enemas
  • Cow’s milk given to infants

Release from cells

  • tumour lysis syndrome
  • Rhabdomyolysis

Reduced excretion

  • CKD** - (4,5)
19
Q

How does hyperphosphataemia present?

A

Binds to plasma calcium ions

  • hypocalcaemia
  • Precipitation in soft tissues: Myocardium, lungs, kidneys

Chronic hyperphosphataemia in CKD causes vascular calcification

20
Q

What individual tests form an LFT profile?

A
  • Total protein
  • Albumin
  • Globulin
  • ALT
  • ALP
  • Bilirubin
21
Q

What are the functions of the liver

A
  • Carbohydrate metabolism - glycogenesis and glycogenolysis
  • Fat metabolism
  • Protein metabolism - albumin synthesis
  • Steroid hormone metabolism
  • Drug metabolism - detoxification of drugs, alcohol, chemicals e.g. ammonia
  • Bilirubin metabolism
  • Production of clotting factors
  • Kupfer cells - macrophage fight infection
  • Storage (glycogen, B12, iron, vit A)
22
Q

What is unconjugated bilirubin

A

When erythrocytes are broken down in the spleen, haemoglobin is separated into Heme (Heme ⇒ Fe2+ & unconjugated bilirubin ) and globin.

Fe2+ and globin are reused in erythropoiesis, the lipid-soluble unconjugated bilirubin (yellow/brown) is excreted.

23
Q

How is unconjugated bilirubin excreted

A
  • Lipid soluble, therefore it is bound to albumin and transported to the liver.
  • Unconjugated bilirubin - albumin complex dissociated
  • unconjugated bilirubin conjugated w/ glucuronic acid ⇒ water-soluble
  • Conjugated bilirubin excreted w/ bile salts into common bile duct into duodenum
  • Conjugated bilirubin (hydrolysed by intestinal flora) ⇒ urobilinogen
  • Some urobilinogen reabsorbed, the rest is converted into stercobilin and excreted as faeces
  • Reabsorbed urobilinogen is excreted by kidneys or converted into conjugated bilirubin to be excreted into bile
24
Q

What liver cells are AST/ALT found in? Where else is AST found? What liver cells are ALP & GGT found? What other cells contain ALP?

A

Hepatocytes contain aminotransferases

AST contained in muscle, heart, kidneys, lungs, leucocytes///

ALP found in:

  • Cells lining bile duct
  • Bone
  • Intestine
  • Placenta

GGT

  • Endoplasmic reticulum of all cells except muscle
25
Q

What are some hepatotoxic drugs

A
  • Paracetamol
  • Methotrexate
  • Amiodarone
  • Isoniazid
  • Statins…
26
Q

What is a good blood test to assess kidney function

A

Prothrombin time

27
Q

How do you tell when alk phos is raised due to liver pathology

A

Raised GGT as well, in skeletal pathology gamma gt doesn’t change

28
Q

What causes raised GGT

A
  • Alcohol
  • Fatty liver/insulin resistance(T2DM)/obesity
  • Drugs
    • Anticonvulsant - phenytoin
    • Warfarin
    • OCP
29
Q

What is the cause of a chronically raised ALT

A

Fatty liver

Alcoholic liver disease

Viral hepatitis

Autoimmune

Haemochromatosis

A1AT deficiency

Phase 3B: Gastroenterology (24 decks)

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