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Medicine PJE > MET > Flashcards

MET Flashcards

1
Q

Rectus sheath above and below arcuate line

A

Above Arcuate Line:
EO passes anteriorly, IO splits and half goes anterior while half goes posterior, TA and transversalis fascia go posteriorly.

Below Arcuate Line:
EO, IO, TA all move anteriorly, TF goes posteriorly.

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2
Q

Blood supply to Abdominal Wall

A

Superior epigastric artery: below the costal margin the internal thoracic artery becomes the SEA

Inferior epigastric artery: comes from the external iliac.

Lateral side supplied by lower IC and lumbar arteries.

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3
Q

Kwashiorkor

A

Protein-wasting malnutrition, micronutrient & anti-oxidant deficiencies

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4
Q

Marasmus

A

Severe malnutrition, muscle wasting, protein loss.

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5
Q

Iron Function, Deficiency and Excess

A 
Function
•	O2 transport
•	Myoglobin function
•	Absorbed in upper small bowel. 
   o	   Transferrin
   o	   Stored as ferritin

Deficiency
• Microcytic anaemia
• Lethargy/fatigue
• Cognitive impairment

Excess
• Haemochromatosis: lethargy, fatigue, diabetes, cirrhosis.

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6
Q

Osteomalacia & rickets

A

Vitamin D Deficiency

Osteomalacia = reduced bone strength, increase in bone fracture, bone pain, bending of bones

Rickets = prior to epiphyseal fusion –> expansion of growth plate and growth retardation

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7
Q

Function of Vitamin D

A

Increases absorption of calcium in the gut

Has two different sources.
o Intake in diet
 Salmon, tuna fish, milk, liver, egg etc…
o Intake through UV sunlight
 Through 7-dehydrocholesterol –> Generates vitamin D3.

If one intake compromised other can compensate.

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8
Q

Wernicke’s Encephalopathy & Korsakoff’s Psychosis

A

Thiamine Deficiency (Vitamin B1)

Wernicke’s Encephalopathy
o Horizontal nystagmus
o Opthalmoplegia
o Cerebellar ataxia

Korsakoff’s Psychosis
o Additional loss of memory and confabulatory psychosis (disturbance of memory)

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9
Q

Beri-Beri

A

Thiamine Deficiency (Vitamin B1)

Dry: peripheral neuropathy (motor and sensory)

Wet: enlarged heart, tachycardia, peripheral oedema, peripheral neuritis

Shoshin: lactic acidosis, cardiac failure

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10
Q

Function of Thiamine (Vitamin B1)

A

Involved in:
o Glycolysis and Krebs cycle
o Branched-chain amino acids metabolism
o Pentose Phosphate Cycle Metabolism

Absorbed in the jejunum.

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11
Q

Pellagra

A

Niacin Deficiency (Vitamin B3)

Early: loss of appetite, irritability, vomiting, abdominal pain

Late: vaginitis, oesophagitis, diarrhoea, depression.
o Casal’s necklace = skin rash (especially in areas exposed to sunlight)

FOUR Ds = dermatitis, diarrhoea, dementia, death.

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12
Q

Function of Niacin (Vitamin B3)

A

Generic form for two forms: nicotinic acid and nicotinamide
o Forms NAD and NADP/NADH and NADPH.

Absorbed in the jejunum.

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13
Q

Types of Feeding

A

Enteral –> oral, nasogastric, orogastric, gastrostomy etc…
• Gastrostomy brain injury, Parkinson’s disease, motor neurone disease

Parenteral –> Peripheral and Central
• Short bowel, small bowel, acute pancreatitis

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14
Q

Blood glucose range before and after meals

A

Kept within range of 3.5-5.5 mmol/L (before meals)

Less than 8mmol/L (2 hours after meals).

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15
Q

Cell in Islets of Langerhans

A
  • Alpha Cells: producing glucagon
  • Beta Cells: producing insulin
  • Delta Cells: producing somatostatin
  • PP Cells: producing pancreatic polypeptide
  • Epsilon Cells: producing ghrelin.
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16
Q

Mechanism of Insulin Secretion

A
  1. If glucose is higher than 5 millimoles it can go through the transporter in the cell.
    a. Ensured by Km of glucokinase (affinity for glucose molecules)
  2. Glucose –> Glucose-6-phosphate –> pyruvate
  3. Generates ATP (rise in ATP: ADP ratio).
    a. Closure of potassium-ATP channels –> Membrane depolarization
  4. Voltage-gated calcium channels open –> Trigger insulin secretion.
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17
Q

Two phases of insulin secretion

A

First phase: rapidly triggered in response to increase glucose

Second phase: sustained, slow release of nearby formed vesicles.

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18
Q

What other substances can trigger insulin release

A

• AAs: arginine and leucine

  • Arginine directly depolarises beta cell membrane
  • Leucine causes allosteric activation activation of GDH
  • Glucagon like peptide-1 (GLP-1)
  • Fatty acids.
  • Acetylcholine.
  • CCK.
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19
Q

Actions of Insulin

A

Glycogen synthesis in muscles (G6P –> G1P –> UDP-glucose –> glycogen)
o Translocation of GLUT4 transporters to plasma membrane

Glucose uptake and lipogenesis (synthesises alpha-glyceryl phosphate –> TGs)

Inhibits lipolysis

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20
Q

How can the liver affect K+ levels

A

Promotes potassium intracellular uptake

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21
Q

Albumin Functions and regular level

A

Large protein synthesised in the liver

o Most abundant protein in plasma and is usually trapped within capillaries (35-50g/l)

Functions to maintain oncotic pressure.

Good indicator of mortality risk
o As inflammation falls albumin level should normalise.

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22
Q

Hypoalbuminemia

A

Arises from inadequate protein intake

In hospital: major cause is inflammation and sepsis associated with infection
 Increased C-reactive protein, white cell count.
 Capillary walls become more porous and albumin drifts out.

NOTE: low albumin DOES NOT reflect poor nutritional status (poor intake).

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23
Q

Blood Supply to the Liver

A

25% through celiac trunk

75% through hepatic portal vein.

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24
Q

What vessels contribute to the portal vein

A

Splenic (inferior mesenteric veins joins here) and superior mesenteric veins meet posterior to head of pancreas to form portal vein

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25
Q

Porto-Systemic Anastomoses

A

Oesophagus:
(P) Left gastric vein and (S) Azygous and hemiazygos

  • Sign/Symptom: Oesophageal varices, hematemesis

Rectum:
(P) Superior rectal vein and (S) Inferior Rectal Vein

  • Sign/Symptom: Recto-anal varices

Anterior Abdominal Wall:
(P) Paraumbilical veins* and (S) Intercostal and inferior epigastric

  • Sign/Symptom: Caput medusa.

Retro-Peritoneal:
(P) Duodenal, pancreatic, right and left colic veins and (S) Lumbar veins

  • Sign/Symptom: Retroperitoneal haemorrhage.
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26
Q

Causes of Ascites

A

fluid in peritoneal space caused by:
• Porta Hypertension, Hypoalbuminaemia
• Aldosterone related renal sodium retention

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27
Q

Venous Drainage of the Oesophagus

A

Oesophageal veins (azygos vein branches)

Left gastric veins (portal vein).

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28
Q

What anatomical structure does the common hepatic duct lie in

A

free margin of lesser omentum

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29
Q

Stimulation of Glucagon Secretion

A

Low blood glucose concentration: 80-90mg/100ml

Increased blood amino acids (alanine and arginine)

Exercise (exhaustive blood concentration of glucagon increases)

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30
Q

What receptor does Glucagon react with

A

G protein-coupled receptor (GPCR)

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31
Q

Process of Glycogenolysis

A

Glucagon activates cAMP which activates PKA

–> Mediates production of glucose from glycogen

Glycogen stores depleted in 24 hours

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32
Q

Process of gluconeogenesis

A

Uses AAs, glycerol and lactate.

Inhibition of phosphofructokinase-1 and pyruvate kinase are critical
 Enzymes in glycolysis.

Increased amino acid uptake into the liver

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33
Q

Process of lipolysis

A

Glucagon activates hormone sensitive lipase
 Allows triglycerides to be broken down.
• Glycerol used in gluconeogenesis.
• Fatty acids used in beta oxidation –> Generate ketone bodies when in excess (Occurs because C substrates in the Kreb’s cycle are used up in prolonged fasting)

Also, involves the activation of the carnitine shuttle
 Transport fatty acids into the mitochondria
• Mediated by CPT-1

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34
Q

Regulation of Glucagon

A

Inhibited: by insulin and somastatin

  • Insulin converts cAMP to 5’AMP through phosphodiesterase –> This switches signalling OFF (does not stimulate PKA).
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35
Q

Catecholamines and Glucocorticoids

A

Both released from the adrenal cortex

Catecholamines = QUICK RESPONSE –> Released in response to stress and hypoglycaemia.
o Synthesized from phenylalanine and tyrosine

Glucocorticoids = LONGER RESPONSE
Cortex cells = have many LDL receptors, enabling cholesterol uptake.
o Enables steroid hormone synthesis

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36
Q

Epinephrine in metabolism

A 
Catecholamine
•	Inhibits insulin secretion
•	Stimulates glycogenolysis in the liver and muscle. 
   o	   Produce cyclic AMP and PKA
•	Stimulates glucagon secretion
•	Increases lipolysis in adipose tissue
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37
Q

Cortisol in metabolism

A

Glucocorticoid
secreted in response to ACTH from pituitary (Negative feedback loop)

o Functions in metabolism
 Enhances gluconeogenesis
 Inhibits glucose uptake
 Stimulates muscle proteolysis
 Stimulates adipose-tissue lipolysis.
 = rapid mobilisation of AAs and FAs from cellular stores

o Resisting Stress and Inflammation
 Maintains blood pressure, suppresses inflammation.
 If prolonged = can induce muscle wasting.

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38
Q

Why do glucocorticoids take longer to cause response

A

It passes through the plasma membrane and binds to nuclear receptor in cell.
• Goes into the nucleus and stimulates transcription of genes.

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39
Q

Thyroid Hormones

A

T4 (thyroxine) and Triiodothyronine (T3)

Activate nuclear receptors and transcription of large number of genes:
 Increases in the number and activity of mitochondria
 Stimulation of carbohydrate metabolism
 Stimulation of fat metabolism

Increased basal metabolic rate

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40
Q

Incretins

A

Group of GI hormones including glucagon-like peptide-1 and gastric inhibitory peptide:
o Enhancement of insulin secretion.

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41
Q

Diabetic causes

A

Obesity:
o Accumulation of lipids and their metabolites
o Increased concentration of circulating FFAs
o Chronic inflammation –> Altered adipokine levels
• Cytokines secreted by adipose tissue
• Lead to chronic inflammation

• Hyperinsulinemia
o Increased lipid synthesis worsens Insulin Resistance

When a tissue is insulin resistant the pancreas tries to create more insulin however the cell doesn’t respond. This increases the synthesis of lipids which makes the whole thing worse.

Both lead to increased insulin resistance –> Diabetes T2

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42
Q

Hyperglucagonaemia in diabetes

A

Occurs even when glucose is high because = alpha cells become resistant to high levels of glucose/insulin through glucolipotoxicity.
 OR defect in insulin secretion.

Nothing to tell cells to stop secreting glucagon

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43
Q

Treatments for:
Decreases Glucose and Gluconeogenesis

Stimulation of Insulin Secretion

Glucagon Peptide 1 Stimulation

A

Decreases Glucose and Gluconeogenesis
• TZD = increases level of transcription of genes.
• Biguanides (Metformin).

Stimulation of Insulin Secretion
• Sulfonylureas
• Meglitidines
o Stimulates closure of potassium channels in beta cells –> increase in calcium –> secretion of insulin.

Glucagon Peptide 1 Stimulation
• Metformin: inhibits DD-4 (molecule usually inhibits G1P) increasing GL1P activation
• Sitagliptin: increases GL1P (stimulates insulin secretion).

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44
Q

What pathway in glucose can excess alcohol inhibit

A

gluconeogenesis is inhibited

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45
Q

Signs and Symptoms for acute hypoglycaemia (only T1D)

A

Mild –> Autonomic: Trembling, sweating, anxiety, hunger

Moderate –> Neuroglycopaenic: Confusion, disorientation, weakness, tiredness

Severe –> confusion, fitting, seizures, coma - Diabetes emergency (mainly for T1D)
 Occurs in patients using blood glucose lowering medication (insulin)
• Missed meal
• Overdose medication.
• Alcohol consumption.

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46
Q

Prolonged Hypoglycaemia

A

Growth hormone and cortisol secreted
o Decrease glucose utilisation and convert to fat utilisation

Leads to: Neuroglycopaenic (shortage of glucose or brain) symptoms

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47
Q

Hyperglycaemia complications

A

Macrovascular
Microvascular

Due to Protein Kinase C Pathway Stimulation

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48
Q

Macrovascular complications of Hyperglycaemia

A

Atherosclerosis
 Increases uptake of LDLs by modification of low LDLD receptor.
 Pro-inflammatory cytokine production

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49
Q

Microvascular complications of Hyperglycaemia

A

o Kidney disease (nephropathy) –> Damage to blood vessels in glomerulus
• Proteinuria, glomerular hypertrophy, decreased glomerular filtration

o Nerve disease (neuropathy) –> 4 types

 Peripheral: pain or loss of feeling in hands, arms, feets and legs

 Autonomic: change in digestion/bowel and bladder control (branches supplying autonomic nerves are affected).
• Also, means don’t have pain (15-20%)

 Proximal: causes pain in thing and hips

 Focal: affect any nerve in the body

o Blindness (retinopathy)

 Non-proliferative: dilation of veins and micro aneurysms

 Proliferative: fragile new blood vessels near optic disk (tend to bleed).

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50
Q

Dyslipidaemia

A

Fat deposition in skeletal muscle –> Worsens insulin resistance

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51
Q

Maturity Onset Diabetes of the Young

A

Pancreatic beta cell dysfunction.

• Inherited (autosomal dominant).

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52
Q

Gestational Diabetes

A

Diabetes in pregnancy
• Increased complications during the second half of pregnancy
• Increased risk of developing T2D

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53
Q

Latent Autoimmune Diabetes of Adults (LADA

A

Antibodies to beta cells.

• Like T1D, Patients become insulin dependent.

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54
Q

Type 3c Diabetes

A

Due to disease of exocrine pancreas

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55
Q

What state of K+ do acidemia and alkalosis lead to

A

acidemia leads to hyperkalaemia

alkalosis leads to hypokalemia

  • H+ enters tissue and binds to protein displacing potassium which exits the cell.
  • H+ leaves cells and potassium enters.
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56
Q

Hyperchloremic metabolic acidosis

A 
Loss of bicarbonate:
CL- compensates (HCO3-/Cl- symporter) for loss
Causes include:
	Severe diarrhoea
	Losses via NG tubes
	Administration of Acidifying Salts.

Reduced Kidney H+ Excretion:
If kidneys do not excrete acids efficiently, bicarbonate is needed to buffer them.
 Bicarbonate travels into the blood and combines with H+
 Exchanged with Cl- to keep charge neutral –> CL- then also exists into the blood (along with K+).

Leads to hyperchloremic metabolic acidosis

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57
Q

Elevated Gap Acidosis

A

Increase in unmeasured anions and decrease in bicarbonate

Causes include:
o Ketoacidosis
o Lactic acidosis
o Renal failure

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58
Q

Low Gap Acidosis

A

Hypoalbuminemia
o Albumin is a negatively charged protein
o Its loss causes retention of bicarbonate and CL to compensate electrical charge.

Causes include:
o	Haemorrhage (loss of albumin through blood) 
o	Nephrotic Syndrome 
o	Intestinal Obstruction 
o	Liver Cirrhosis
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59
Q

Ammonium production (kidney)

A

titratable acids –> H+ + HPO42- –> H2PO4- and ammonium (NH4+)

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60
Q

Action of these kidney cells:
Alpha-intercalated
Beta-intercalated

A

Alpha-intercalated = secrete acid, reabsorb bicarbonate

Beta-intercalated = secrete bicarbonate, secrete acid

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61
Q

Glutamate Pathway in acidosis

A

Allows to produce bicarbonate (production of alpha-ketoglutarate to glucose = side products are NH4+, HCO3-)

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62
Q

Hormonal Regulation of the Acid/Base Status

A

Aldosterone = increases pH

Angiotensin II = increases PH

Parathyroid = prevents reabsorption of HPO42 and increases pH

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63
Q

Orexigenic peptide and neurons

A

Agouti Related Peptide (AgRP)

NPY Neuron

Melanocortin receptor antagonists –> Inhibit the satiety centre.
o Appetite stimulating

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64
Q

Anorexigenic peptide and neurons

A

Proopiomelanocortin (POMC)

(Cocaine, Amphetamine Regulate Transcript (CART) Neuron

Melanocortin receptor agonists –> POMC undergoes post-translational modification –> melanocortins (Stimulate satiety centre)
o Appetite inhibiting.

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65
Q

Alpha-melanocyte-stimulating hormone (MSH)

A

Predominant POMC derived products

If deficient will result in hyperphagic (abnormally great desire for food) obesity

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66
Q

Anorexigenic peptides

A

Serotonin (5HT) = anorexigenic
• Acts through Htr1b and HTr2c receptors that increase signalling from POMC neurons
• Htr1b decreases AgRP neuron signalling
o These receptors interact with ARC (arcuate nucleus)

PPY 3-36 = anorexigenic
• Synthesized in gut. 
• Mechanism of action
   o	Inhibits NYP neurons (Y2 receptors)
   o	Stimulates POMC neurons 
   o	Decreases food intake.

GLP-1 and PPY = anorexigenic
• Released by cells in the gut lining
o Inhibits NYP and stimulates POMC.

Cholecystokinin = anorexigenic
• Secreted from I-type enteroendocrine cells in duodenum and SI

Leptin = long acting anorexigenic
• Secreted by adipose tissue (amount of leptin = amount of adipose tissue).
o Indicates total energy storage.
• Pattern: start with relatively low leptin during the day. It rises and starts to fall at night.
o Fasting causes a decrease in leptin

ALSO Drop AGRP levels

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67
Q

Malonyl CoA

A

Potent controller of appetite
o Inhibits lipolysis (carnitine shuttle) at high levels
o Lipolysis is stimulated at low levels.

Not Hungry = result of malonyl-CoA increased in cytoplasm (for FA synthesis) –> High levels sensed by hypothalamus
• Turns down AgRP and NPY
• Decreases appetite.

Hungry = less malonyl-CoA in cytoplasm (no FA synthesis) –> Sensed by hypothalamus
• Increases AgRP and NPY.

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68
Q

Insulin contribution to Obesity

A

It decreases the rate of lipolysis in adipose tissue (and lowers plasma fatty acid level).
o Increases uptake of TGs from blood into adipose tissue

Stimulates FA and TG synthesis in tissues.

Decreases rate of fatty acid oxidation in muscle and liver.

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69
Q

T2D Drugs on Insulin Levels:
Increase
Stable
Decrease

A

Increase:
insulin injections, sulfonylureas – increases insulin release
TZD – increases level of transcription of genes

Stable:
metformin
DPP IV inhibitors

Decrease:
SGLT-2 inhibitor – SGLT-2 in the kidney to help reabsorb glucose

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70
Q

Thrifty gene hypothesis

A

Selective advantage of obesity in populations with frequent starvation

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71
Q

Syndromic Monogenic Obesity

A

Mental retardation, dysmorphic features in addition to obesity

Bardet-Biedl Syndrome - Ciliopathy
 Cilia mediate leptin receptor signalling

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72
Q

Polygenic Obesity

A

Involves CNS, food sensing and digestion, insulin signalling, lipid metabolism, muscle and liver biology, gut microbiota as well as:

Adipocyte Differentiation
• Ciliopathies
• Mutations in PPARy2.
o Targeted by TZD drugs.

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73
Q

Main site of adaptive thermogenesis

A

Brown Adipose Tissue

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74
Q

Orlistat

A

lipase inhibitor

o Reduces amount of fat absorbed from food

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75
Q

Wolffian and Mullerian ducts

A

Mesonephric = Wolffian Ducts (precursor male internal sex organ)

Paramesonephric = Mullerian Ducts (precursor female internal sex organ)

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76
Q

Embryonic Kidneys

A

Pronephric
Mesonephric
Metanephric

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77
Q

Ascent of the Kidney

A

Metanephros located in the sacral region (S1)

Ascends as the embryo unfolds –> To the lumbar region (T12)

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78
Q

Function of the Kidney Within Foetus

A

Involved in generation of amniotic fluid

Functional at the end of the first trimester.

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79
Q

Kidney Agenesis

A

Failure of kidney to form
unilateral
bilateral (baby will not survive after birth)
 Oligohydramnios = reduction in amniotic fluid.
 Birth defects = lung development and club foot

80
Q

Polycystic Kidney

A

Kidney develop fluid filled cysts
 Cysts originates as dilations of intact tubule
 Cysts enlarges and loses contact with nephron
 Cysts epithelium becomes secretory resulting in increased fluid secretion.
 Increased proliferation of cyst epithelium.

81
Q

Types of Polycystic Kidney

A

Autosomal dominant (polycystin mutation):
 85-90% are polycystin (PKD-1) mutations
 10-15% are polycystin-2 (PKD-2) mutations.
• Polycystin = localised to primary cilia –> Involved in cell adhesion, calcium transport, cell cycle

Autosomal recessive (fibrocystic mutation)

82
Q

Vessels in Drainage of Urine

A

Collecting ducts –> renal papilla –> minor calyx –> major calyx –> renal pelvis –> ureter

83
Q

Internal Vasculature of the kidneys

A

Renal artery –> 5 segmental arteries (each supply renal segments)

Segmental arteries –> interlobar arteries –> arcuate –> interlobular arteries –> afferent arterioles –> glomerular capillaries

Capillaries –> interlobular veins –> arcuate veins –> interlobar veins –> renal vein.

84
Q

Blood Supply to the Kidney

A 
Renal arteries (L1/L2): 
o ¼ of cardiac output. 
o RRA passes posteriorly to IVC
Renal veins (L2)
o Anterior to aorta 
   	LRV longer than right due to right --> Receives left suprarenal and gonadal veins
85
Q

Lymph drainage from the kidneys

A

Lateral aortic lymph nodes

86
Q

Nerve Supply and pain in the kidneys

A

Via the renal plexus
o MOTOR
 Sympathetic (visceral afferent)

87
Q

Blood Supply to Ureters

A

Renal arteries
Testicular arteries
Common iliac arteries.

88
Q

Structure of Ureter

A

Tri-layered wall:
o Transitional epithelial mucosa.
o Smooth muscle muscularis.
o Fibrous connective tissue adventitia

Muscle for peristalsis

89
Q

Pain in Ureter/Kidney stones)

A

Referred along ilioinguinal and Iliohypogastric nerves (L1)

Descent –> may start to feel pain over groin
- nerve change –> Pain referred to genitofemoral (L1/L2)

90
Q

Trigone

A

Area between ureters and urethra

infections persist in this region

91
Q

Structure of Bladder

A
  • Transitional epithelial mucosa
  • Thick muscular layer
  • Fibrous adventitia
92
Q

Urethra Sphincters

A

Urethra = Muscular tube

o IUS = involuntary sphincter (male) - prevents retrograde ejaculation

o EUS = voluntary sphincter

o Levator ani = voluntary urethral sphincter

93
Q

four sections of Urethra in males

A

Intramural (pre-prostatic) = length varies on bladder filling

Prostatic = contains ejaculatory ducts

Intermediate (membranous) = penetrates perineal membrane
• Surrounded by EUS.

Spongy = final part in corpus spongiosum of penis.

94
Q

Micronutrition (Voiding or Urination)

A

Distension of bladder walls initiates spinal/sympathetic reflexes:
o Stimulate contraction of EUS.
o Inhibit detrusor muscle and IUS

Voiding reflex: parasympathetic
o Stimulate detrusor muscles to contract
o Inhibit internal and external sphincters.

SYMPATHETIC STOPS PEE

PARASYMPATHETIC PERMITS PEE

95
Q

Measurement of GFR

A

Done by creatinine = completely filtered and none is reabsorbed.
o Break-down produce of Creatine Phosphate found in muscle

96
Q

Cr Clearance

A

(urine concentration x urine volume)/plasma concentration

Creatinine is also actively secreted leading to an overestimation of 10-20%

Misleading in:
• Muscular individuals (naturally raised serum creatinine)
• Malnourished individuals = low serum creatinine.
• Drugs = may inhibit tubular secretion of creatinine (e.g. Trimethoprin)

97
Q

Gold standard of GFR

A

A nuclear medicine scan (e.g. Cr51-EDTA)

98
Q

Renal Disease and Transport Proteins

A

Proximal tubule:
o Apical Na/cysteine cotransporter = cystinuria
o Apical Na/glucose cotransporter = renal glycosuria
o Basolateral Na/HCO3 = proximal RTA

Thick Ascending Loop = Bartter Type 1

Distal Tubule = Gitelman’s

99
Q

Reabsorption of Proximal, distal Tubule and loop

A

Proximal Tubule:
Bulk reabsorption of solutes to 80%, water 65%, AAs, low molecular weight Ps (100%)

Loop of Henle:
• Descending - many aquaporins - allow water to move out –> more conc.
• Ascending - active transport of sodium and chloride out of the tubule
 Secondary Active Transport = Na, K and CL
 Paracellular Transport: Na, Ca Mg down concentration gradient

Distal Nephron:
Excrete potassium, regulate sodium delivery to collecting duct as well as urine acidification

100
Q

Effects of Glucose Presence in Urine

A

Osmotic diuresis

o Water and urine attracted into collecting duct due to increased solute –> leads to polyuria.

101
Q

Glucose renal threshold

A

> 10 mmol/L.

102
Q

Cushing’s Syndrome/Disease

A

Syndrome: high cortisol

Disease: high cortisol caused by tumour that causes increased ACTH secretion

Symptoms:
o Loss of peripheral vision
o Progressive Opthalmoplegia 
   	Paralysis of muscles within/surrounding eyes.  
o Weight gain (truncal obesity)
o Abdominal striae.
103
Q

Sella turcica

A

Depression in the sphenoid where Pituitary sits

104
Q

Anterior Lobe Hormones

A

o ACTH = adrenocorticotrophic hormone
EXCESS = Cushing’s syndrome/disease.

o TSH = thyroid-stimulating hormone
EXCESS = hyperthyroidism, weight loss, rapid heart rate, tremors.

o LH = luteinising hormone

o FSH = follicle-stimulating hormone
EXCESS = irregular menstrual periods and decreased interest in sex

o PRL = prolactin
EXCESS = irregular menstrual periods, abnormal milk production.

o GH = growth hormone
EXCESS = gigantism, acromegaly in adults.

o MSH = melanocyte-stimulating hormone.

105
Q

Posterior Lobe Hormones

A

Extension of the hypothalamus (made up of neural tissue)

Two nuclei = cell bodies extend down into the Posterior Pituitary 
o Supraoptic (above the optic chiasm) 
   	ADH 
o Paraventricular nuclei. 
   	Oxytocin
106
Q

Adrenal Gland shapes

A

Right AD = pyramidal shaped right (contact with liver and IVC)

Left AD = crescent shaped left (spleen, stomach, pancreas).

107
Q

Blood Supply

A

Superior suprarenal artery (6-8) = inferior phrenic

Middle suprarenal artery (1+) = abdominal aorta

Inferior suprarenal artery (1+) = renal artery.

Venous drainage on the left is into the renal vein, on the right on the IVC

108
Q

Damage to what in surgery causes tetany

A

Parathyroid glands

109
Q

Level of Thyroid Gland

A

C5-T1

110
Q

Arterial Blood Supply to Thyroid Gland

A

ECA = superior thyroid artery

Subclavian –> thyrocervical trunk = inferior thyroid artery

Common variant: thyroid IMA artery (10%)

111
Q

Venous Blood Supply

A

IJV = Superior, middle thyroid vein.

BCV = Inferior thyroid vein.

112
Q

Blood Supply to pancreas

A

Coeliac Trunk
 Splenic artery
 Gastroduodenal –> superior pancreatoduodenal (when it gives of its final gastric branch)

Superior Mesenteric Artery
 Inferior pancreatoduodenal.

113
Q

Iodine required in diets

A

1mg

114
Q

Synthesis of Thyroid Hormones

A
  1. Iodide taken up by NIS (sodium-iodine symporter on basolateral membrane of thyroid follicular cell) Release tyrosine molecules from structure.
    b. Causes T3 and T4 to separate.
    c. DIT and MIT release iodine to restart process
115
Q

Action of Thyroid Hormones

A

T3 enters the nucleus (converted from T4) and enters target cells
• In the nucleus = thyroid hormone receptor.

Initiates transcription for specific mRNAs.
• This increases the metabolic rate.

116
Q

Thyroid Deiodinases

A

D1 = rT3 –> T4 –> T3

D2 = provide T3 to the nucleus
• T4 levels fall = D2 is upregulated –> T3 levels are maintained
• (If no longer able to compensate = rise in TRSH/TSH).
• Excess T4 = decrease D2 to protect from excess thyroid hormone

D3 = activated by ischemia/hypoxia, slowing down metabolism of affected tissues by reducing T3 levels.

117
Q

Hyperthyroidism (hyper function of the thyroid gland)/ Thyrotoxicosis symptoms

A

CV
• Atrial fibrillation (dissipate heat)

NS
• Nervousness seizures

Eyes
• Eyelid retraction
• Inflammation of orbital soft tissue (buldging).

Skin
• Plummer’s Nails
• Pretibial myxoedema

Bones
• Accelerated osteoclast activity
• Hypercalcemia
• Osteoporosis

Metabolism
•	Increased protein and lipid degradation
•	Increased appetite
•	Heat intolerance
•	Hyperglycaemia.

Haematological
• Pernicious anaemia – RBC deficiency
• B12 deficiency

Reproduction
• Oligomenorrhea – infrequent periods
• Gynecomastia – enlargement of male breast’s
• ED

118
Q

Grave’s Disease

A

An autoimmune thyroid disease

Positive antibodies against TPO, thyroglobulin and most significantly the TSH receptor

119
Q

Causes of Hyperthyroidism (hyper function of the thyroid gland)/ Thyrotoxicosis

A
  • Grave’s Disease
  • Toxic multinodular goitre – swelling in the thyroid gland
  • Toxic adenoma – noncancerous tumour
  • Excess iodine
  • HCG
120
Q

Diagnosis and Management of Hyperthyroidism

A

Diagnosis: High T3 and T4

Treatment: Thionamide drugs
• Propylthiouracil.
• Carbimazole.

121
Q

Primary and secondary Hypothyroidism

A

Primary - loss of thyroid
Central or secondary - insufficient pituitary stimulation (commonly pituitary macroadenoma affecting anterior pitruitary)

122
Q

Hypothyroidism symptoms

A

CV
• Reduced cutaneous circulation = sensitivity to cold
o J waves (wave directly after S) of hypothermia
• Sinus bradycardia

GI Tract
• Reduced appetite constipation.
• Weight gain

Nerves, muscle, bone
• Impaired fetal brain development
• Dementia
• Growth retardation

Endocrine
• Delayed puberty
• Erectile dysfunction

Metabolism
• Reduced BMR
• Decreased GLUT4 stimulation

Renal
• Reduced GFR
• Mild hyponatraemia

Haematological
• Normochromic/normocytic anaemia

123
Q

Causes of hypothyroidism

A

Hashimoto’s disease

Infiltrative disease

Hypopituitarism – pituitary doesn’t produce sufficient (if any) hormones

Cabbage – in iodine deficiency

Lithium.

124
Q

Diagnosis and Management

A

Diagnosis = high TSH, low T4

Treatment
• Levothyroxine
• Liothyronine

125
Q

Embryonic structure origins

A

Endoderm = lung cells, thyroid, digestive cells.

Mesoderm = cardiac muscle, skeletal muscle, tubule of the kidney, RBCs
• Visceral mesoderm wraps around gut tube.
o Forms mesenteries (suspend the gut tube in body cavity).

Ectoderm = skin cells, neurons of the brain pigment.

126
Q

What is Hirschsprungs Disease and symptoms

A

Congenital megacolon due to lack of enteric neurons (ENS)
o Affected segments can’t relax (don’t allow stools to pass) – no peristalsis

Symptoms:
o Failing to pass meconium within 48 hours
o A swollen belly
o Vomiting green fluid.

127
Q

Anal Sphincters

A

Internal Anal Sphincter (IAS):
• Involuntary and thickened muscle

External Anal Sphincter (EAS):
• Voluntary muscle which encircles the IAS
o Lies just below and laterally to the lower edge of the IAS

• Defers defecation until a socially opportune moment.

128
Q

Nerve supply to Pelvic Floor Muscle

A

S2-S4 give parasympathetic supply through the pudendal nerve.
o Keeps the 3Ps off the floor (penis, poo and pee).

129
Q

Anal sphincter nerve supply

A

External Anal Sphincter:
Supplied by the inferior rectal branch of the pudendal nerve. Further divides to form the
o The perineal nerve and dorsal nerve of the penis.
o Dorsal nerve of the clitoris

Internal Anal Sphincter:
Innervated by the enteric nervous system (ANS)
o Sympathetic: L1, L2 via hypogastric nerves
 EXCITATORY (STOP)
o Parasympathetic: S2-S4 pelvic nerves
 INHIBITORY (LET GO)
In a continuous tonic state

130
Q

Constipation types

A

Primary and secondary

131
Q

Primary Constipation

A

Normal Transit
• Patient feels constipated.

Slow Transit
• Infrequency and slow movement of stool.
• Bloating, abdominal pain and infrequent urge to defecate

Disordered Defecation
• Dysfunction of pelvic floor and anal sphincters (due to structural abnormalities).

132
Q

Secondary Constipation

A

Endocrine = diabetes (high blood sugar damages vessels), hypothyroidism

Neurological = spinal injury: Parkinson’s disease

Psychogenic = eating disorders

Metabolic = hypercalcaemia etc…

133
Q

Passive Incontinence

A

Structural/functional lesion to the internal sphincter.

134
Q

Urge Incontinence

A

• Structure/functional lesion to the external sphincter

135
Q

Acidotic State and Ca2+

A

less calcium binds to albumin (replaced by H+): increase in ionized Ca2+.

136
Q

Alkalotic State and Ca2+

A

More calcium binds to albumin, decrease in ionized Ca2+

• Causes tingling of the lips (hypocalcaemia due to blowing of Co2).

137
Q

is Hypocalcaemia or hypercalcaemia more dangerous

A

Hypocalcaemia = causes uncontrolled firing of nerves across the body (more dangerous than hyper).
o Can cause cardiac arrhythmia’s/cardiac arrest.

138
Q

Calcium role in signalling

A

Intracellular circulating molecule that is also involved in stabilizing Na+ pumps
o Sits within these channels to prevent them from firing.

139
Q

Where is phosphate mineralised

A

85% is mineralised in bone.

140
Q

PARATHYROID HORMONE

A

Secreted PTH in response to low calcium.
o PTH Secreted by Chief Cells

Causes an increase in extracellular calcium through:
o Bone = increases activity of osteoclasts (bone reabsorption –> releases more Ca2+/PO43)

o Kidney = increases Ca2+ reabsorption, decreases phosphate reabsorption –> Phosphate forms salts with calcium and decreases the amount that is ionized

o Intestine = increased hydroxylation of vit. D to produce calcitriol (1,25-dihydroxyvitamin D) –> Calcitriol promotes reabsorption of calcium through gut by stimulating CBP.

141
Q

PTH Regulation

A

High levels of calcium inhibit PTH (minor change)

However a basal amount secreted.

142
Q

Familial Hypocalciuric Hypercalcemia

A

Inactivating mutations of CaSR.
o Parathyroid can’t sense high calcium
o PTH not supressed.

High serum Ca, low urine Ca (reabsorption not stopped)

143
Q

Determinants of PTH Secretion

A

Decrease Secretion:
• High Calcium
• Activated vitamin D (1,25D/calcitriol) from 25 (OH) D3: supresses PTH transcription.
o Negative feedback loop
• Cinacalcet activates Calcium Signalling Receptors = restrains PTH

Increase Secretion
• Phosphate (increased secretion).

144
Q

Where does PTH act

A

PTH only acts on distal tubule

o Upregulates TRV calcium channels/calcium ATPase and Na/Ca exchanger.

145
Q

Osteoblasts

A

Contain and produce RANKL.

o PTH and 1,25D stimulate RANKL production.

146
Q

Osteoclasts

A

Have RANKL receptors
o RANKL activation: forms seals over bone and cause its breakdown (release H+) –> Release Ca2+

OPG (osteoprotegerin) inhibits this process and is therefore downregulated by PTH

147
Q

Further factors of bone Remodelling

A

Glucocorticoid = reduce osteoblast number, increase RANKL.

Estrogen = inhibits bone remodeling.

148
Q

How is 1,25 (OH)D made

A 
Vitamin D (Absorbed by diet or UV light)
o	Undergoes hepatic conversion to 25(OH)D.

Conversion to 1,25 (OH)D is highly regulated.

149
Q

Function of 1,25 (OH)D

A

Increase Ca2+ and phosphate absorption from the gut.
o And from kidney

Stimulates bone reabsorption and remodeling

Other Effects
• Increases levels of osteocalcin and RANKL
• Increases amino acid uptake.

150
Q

FGF23

A

Secreted by osteoblasts in response to high phosphate levels.

Decreases Ca2+ and phosphate levels.

151
Q

Calcitonin

A

Thyroid C-cells (secrete calcitonin)

Medullary thyroid cancer (levels of calcitonin increase –> marker)

152
Q

PTHrP

A

Physiological role in lactation

153
Q

HYPERPARATHYROIDISM Complications

A

stones (renal calculi)
bones (osteoporosis)
groans (dyspepsia – indigestion pain in upper abdomen after eating)
moans (depression, confusion)
polyuria and polydipsia (increased thirst)

154
Q

Primary, secondary and tertiary HYPERPARATHYROIDISM

A

Primary disease (parathyroid adenoma, carcinoma hyperplasia)  hypercalcemia (no lack of Ca2+)

Secondary disease (compensates for decreased Ca2+ by increasing PTH)

Tertiary disease is caused by successful compensation of chronic secondary hyperparathyroidism.

155
Q

HYPOPARATHYROIDISM symptoms

A

Features:
o Convulsions.
o Arrhythmias.
o Seizures.

156
Q

Rathke’s pouch

A

Ectoderm that grows from the roof of the mouth (forms anterior pitruitary)

157
Q

Posterior pituitary formation

A

from the diencephalon of the brain

158
Q

Oxytocin

A

Stimulates milk synthesis

159
Q

ADH/Vasopressin

A

Increases water absorption through the opening aquaporins in the collecting duct

Desmopressin = drug that mimics it.

160
Q

Iliothyronine

A

synthetic form of T3

161
Q

What stimulates GH

A

GHRH as well as ghrelin

o Inhibited by SS (negative feedback = secreted when there are high levels of GH)

162
Q

What does GH stimulate

A

Stimulates IGF (insulin-like growth factor) production.
o Inhibits GF and GFHRH via negative feedback.
o Stimulates secretion of SS.

163
Q

McCune-Albright Syndrome

A

Spontaneous mutation in the embryo.
o Prevents downregulation of cAMP in GCPRs

Results in:
o Hyper functioning endocrine organs (goitre)
o Bone deformities.
o Skin discolorations (often to café au lait [orange] color).

More common in females.

164
Q

Hypothalamo-Pituitary-Adrenal Axis

A

CHR–> ACTH –> cortisol

negative feedback

165
Q

Circadian Rhythm of Cortisol

A

Rise at about 3am
Peak at 6-9am
Levels decline throughout the day

166
Q

Cushing’s Syndrome and types

A

Increased cortisol levels
Two types:

ACTH Independent:
 ACTH not being impact.
 Adrenal tumour may be the cause
• Cause of raised cortisol downstream from the pituitary gland.

ACT Dependent:
 ACTH levels raised primarily.
 Issue due to a pituitary defect (e.g. adenoma).
• Increased ACTH leads to increased cortisol.

167
Q

Cushing’s Syndrome symptoms

A

Weight gain
muscle weakness
skin changes

168
Q

Gonadal Axis

A

Kisspeptin stimulates GnRH (gonadotropic releasing hormone) in the hypothalamus

GnRH stimulates LH and FSH in the pituitary glands

This causes oestrogen and testosterone production in the gonads.
o Inhibit Kisspeptin and LH/FSH via negative feedback

in puberty oestrogen causes positive feedback to Kisspeptin

169
Q

Classes of Diuretics

A

Carbonic anhydrase inhibitors - Proximal Convoluted Tubule (bicarbonate ions are not reabsorbed)

Thiazide Diuretics - Distal Convoluted Tubule
(block the Na+/Cl- –> decreases Na+ reabsorption to cause diuresis)

Loop Diuretics - Ascending Limb of Loop of Henle (inhibits the Na/K/2CL co-transporter –> K+ excretion)

Potassium Sparing Diuretics - Collecting Tubules (Lose Na+ and gain K+)

  • Amiloride/Triamterene
    Na+ channel antagonists –> Na+ loss - diuresis
  • Spironolactone/Eplerenone
    Aldosterone antagonists therefore deregulates Epithelial Sodium Channels (ENaCs) –> Na+ loss - diuresis
170
Q

Mannitol

A

Osmotic Diuretic
• Na+, K+ and water are all dragged out from the interstitial space

Clinical Use:
• Cerebral oedema / raised intracranial pressure.

Side Effects:
• Pulmonary oedema.

171
Q

Micturition Reflex

A

Micturition centre activated
• (1) Stimulation of parasympathetic efferents (stimulate detrusor muscle to contract).
o Action continued through positive feedback.
o Release acetylcholine which stimulate muscarinic receptors on smooth muscle.

• (2) Inhibition of somatic efferents (pudendal nerve) and sympathetic efferents (hypogastric nerve)
o Relaxation of sphincters and detrusor muscle

172
Q

International Prostate Symptoms Score

A 
Involves frequency, urgency, nocturia etc…
o	Mild (0-7) = reassure, watch and wait 
o	Moderate (8-19) to Severe (20-35)
173
Q

Lower Urinary Tract Symptoms (LUTS)

A

Storage (Irritative) Symptoms = frequency, nocturia, urge incontinence

Voiding (Obstructive) Symptoms = hesitance, straining, poor flow, incomplete emptying (also = terminal dribbling, haematuria)

Overactive Bladder Syndrome (OAB) = urgency, with or without incontinence (usually with frequency and nocturia).

174
Q

Medical Therapy for Lower Urinary Tract Symptoms (LUTS)

A

Alpha blockers (stretchers)
o Prevent activation of alpha receptors (which activate smooth muscle).
 Enlarges lumen of urethra.

5-alpha reductase inhibitors (shrinkers)
o Reduce growth of prostate.
 Enlarges lumen of urethra

PDE5 inhibitors.

Antimuscarinics.

175
Q

Surgery for Lower Urinary Tract Symptoms (LUTS)

A

TURP = transurethral resection of the prostate

HoLEP = laser to remove prostate

UroLIFT = holds prostate gland out of the way

176
Q

Urge Incontinence

Stress Incontinence

A

Urge Incontinence = overactive waves (overactive bladder)

Stress Incontinence = urine leaks due to weakened pelvic muscles

177
Q

Treatment for Urge Incontinence

A

Anticholinergics = block Ach in parasympathetic nerves (as well as in other places)

Beta adrenergics = beta receptors upregulated in OAB. Decrease this but hypertension.

Botulinum Toxin A = fuses synaptic vessels with end plate.
 Issues with hyper continence.

178
Q

Mineralocorticoids

A

Involved in electrolyte and water balance.

179
Q

Glucocorticoids

A

Affects metabolism, fights infection (anti-inflammatory), prevents fluid loss, affects neurochemistry etc…

180
Q

Side Effects of Glucocorticoids

A
  • Oedema
  • Weight gain
  • Hypertension
  • Osteoporosis (increases activity of osteoclasts, decreases activity of osteoblasts).
  • Hyperglycaemia
  • Glaucoma
  • Jaundice
  • Peptic ulcers (sore on lining of stomach/SI/eosophagus)
  • Avascular necrosis
181
Q

Use of Glucocorticoids

A
  • Hypersensitivity such as asthma, atrophic dermatitis (eczema) and allergic rhinitis (nose allergy)
  • Adrenal deficiencies
  • Chron’s disease or ulcerative colitis
  • Arthritis
  • Multiple sclerosis.
182
Q

Glucocorticoid Receptors

A

Alpha and beta are the two main forms

Found within nucleus and cytoplasm
o Can enter through cell membrane as they are lipid.

183
Q

Synthetic Forms of Glucocorticoids

A
  • Dexamethasone
  • Betamethasone
  • Prednisone
  • Prednisolone.
184
Q

Acute Cellular Rejection

A

CD4+ activate cytotoxic T lymphocytes (CD8+).

o “Cell-mediated”

185
Q

Acute Antibody-Mediated (Humoral) Rejection

A

CD4+ activate B lymphocytes that produce antibodies

o Gives a different type of pathology.

186
Q

what is used to identify rejection.

A

C4d levels

187
Q

Cellular vs Antibody Rejection

A

Cellular: More c4d between cells/connecting cells

Antibody: around the blood vessels (peritubular)

188
Q

Hyperacute Rejection

A

Minutes to hours.

Antibodies in the circulation before the transplant occurs.

189
Q

Chronic Rejection

A

Occurs from months to years

190
Q

Immunosuppression in Rejection

A

Acts to prevent activation of helper T cells.

Activated T cells secrete IL to cause clonal expansion

Corticosteroids: prevent cytokine gene activation

191
Q

Chromaffin cells

A

Release catecholamines (80% secrete adrenaline, 20% noradrenaline)

192
Q

Steroid production

A

Cholesterol conversion through cytochrome p450 to pregnenolone initiates pathway.

193
Q

Hyperaldosteronism signs

A

low potassium, high blood pressure and alkalosis

194
Q

Functions of Aldosterone

A

Stimulates Na/K ATPase and increases its expression.

Inserts additional ENaC.

Stimulates the H+ ATPase

195
Q

Liddle’s Syndrome

A

Increased expression of ENaC:
• Hypertension
• Hypokalemia
• Metabolic Alkalosis

196
Q

Addison’s Disease

A

Primary Adrenal failure: can be autoimmune and tuberculosis

Vague symptoms initially
o Fatigue, weakness, myalgia
o Anorexia, weight loss
o Hyperpigmentation.

197
Q

Chromaffin Cell Tumours

A

Phaeochromocytoma: arising from within adrenal medulla

Paraganglioma: extra-adrenal tumours.
Known as PPGL

Medicine PJE (7 decks)

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