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MEH (Milly's) > Key Conditions > Flashcards

Key Conditions Flashcards

1
Q

Name some causes of malnutrition? (4)

A
  1. Malabsorption (Crohn’s disease etc)
  2. Eating disorders (anorexia nervosa etc)
  3. Lack of food availability
  4. Unable to adequately feed oneself (disability etc)
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2
Q

What is Marasmus?

A

A condition in which someone is severely underweight due to calorie and protein deficiencies.

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3
Q

What is the appearance of someone with marasmus?

A

Muscle wasting
Emaciated
Loss of body fat
Normal hair

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4
Q

What is kwashiorkor?

A

A condition resulting in ascites and oedema due to low protein intake

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5
Q

How does kwashiorkor result in oedema?

A

Low oncotic pressure due to decreased serum protein production (ie albumin), this means tissue fluid is not returned to capillaries

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6
Q

How does kwashiorkor lead to hepatomegaly?

A

Lack of amino acids for transport proteins therefore there is less fat transport which results in fatty liver build up, there is also less fat breakdown which further exacerbates the problem

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7
Q

What are features of someone with kwashiorkor? (6)

A 
Thin, pale, weak hair
Mild anaemia 
Thin limbs 
Hepatomegaly
Oedema (ascites)
Flaking rashes
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8
Q

What is the BMI of someone who is clinically obese?

A

> 30

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9
Q

What is the BMI of someone who is morbidly obese?

A

> 35

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10
Q

What is obesity a risk factor for? (5)

A 
Type 2 diabetes
CHD-atherosclerosis 
Osteoarthritis 
Cancers 
Psychological damage (negative body image)
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11
Q

What causes obesity?

A

Excessive energy intake (stored in adipose tissue)

Excessive alcohol and fat intakes

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12
Q

How is obesity managed?

A

Exercise and reduction in fat content

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13
Q

What is galactosaemia?

A

Inability to utilities galactose by the body leading to excessive levels in the blood

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14
Q

What are the 3 types of galactosaemia?

A

Type 1: deficiency in galactose 1-P uridyl transferase enzyme (second enzyme in pathway)
Type 2: deficiency in galactokinase enzyme (first enzyme in pathway)
Type 3: deficiency in UDP galactose epidermase enzyme (3rd enzyme in the pathway)

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15
Q

What are signs and symptoms of type 1 galactosaemia and why?

A

Jaundice, vomiting, diarrhoea, high blood sugar, low blood glucose, galactosuria, cataracts

Why?: In the absence of galactose 1-P uridyl transferase there is a build up of galactose 1-P which is toxic to hepatocytes, there is also a backing up of the pathway and the galactose levels also increase

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16
Q

What are the clinical features of type 2 galactosaemia? Why?

A

Cataracts and other small issues (ie galactosuria)

Why?: the body deals with the high galactose levels by converting it to the sugar alcohol galactitol, this process requires NADPH, with decreased NADPH levels there is no maintenance of cysteine residences and cataracts is caused

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17
Q

What is the treatment for galactosaemia?

A

Remove lactose from diet

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18
Q

What is the mechanism behind jaundice?

A
  1. Damage to liver
  2. Red blood cells broken down producing bilirubin
  3. Less bilirubin is conjugated (due to liver damage), it remains insoluble
  4. Unconjugated bilirubin builds up and it released into blood
  5. As it is insoluble, it moves into tissues
  6. Gives yellow colour to skin
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19
Q

What is lactose intolerance?

A

The deficiency of the enzyme lactase

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20
Q

How does a lack of the lactase enzyme cause issues?

A

Lactose is unable to be broken down in the gut so remains
Bacteria colonises the un-hydrolysed lactose and ferments it to produce organic acids that irritate GI. This can cause stomach cramps and diarrhoea

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21
Q

How is lactose intolerance treated?

A

Remove lactose from diet (avoid most dairy products)

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22
Q

A G6PDH deficiency leads to reduced NADPH production, what effect does this have? (4)

A
  1. reduction of lipid synthesis
  2. Less maintenance of SH residues in lens of eye- cataracts
  3. Less maintenance of SH residues in RBC therefore disulphide bonds form- Heinz bodies
  4. Glutathione reduction- important in RBCs etc for ROS detoxification
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23
Q

What are the symptoms of lactic acidosis?

A

Rapid Deep breathing
Abdominal pain
Nausea

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24
Q

When would lactic acidosis occur?

A

As a result of anaerobic respiration
Reduction of pyruvate by lactate dehydrogenase

When excess intracellular lactate is released into the blood, maintenance of electroneutrality of the blood requires that a cation be released into the blood, as well. This can reduce blood pH

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25
Q

What is the result of any TCA cycle defect?

A

Death

Lack of any enzyme is not compatible with life

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26
Q

Give 2 examples of uncouplers

A

Dinitrocresol

Dinitrophenol

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27
Q

How do uncouplers work?

A

Increase permeability of membrane to protons
Dissipation of pmf as heat, protons bypass ATP synthase
Uncoupling of ETC and OxPhos

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28
Q

How does brown adipose tissue use uncouplers?

A

Uses action of UCP1 to allow non-shivering thermogenesis

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29
Q

What is the pathophysiology of cyanide poisoning?

A

Blocks the ETC by bind to the electron transport proteins to prevent the oxidation of NADH and FADH2
No pmf established due to inactivity of proton translocation complexes

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30
Q

What are the consequences of have too much glycogen stored?

A

Tissue damage in liver and muscle

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31
Q

What are the consequences of having too little glycogen storage?

A

Poor exercise tolerance

Hypoglycaemic tendencies during fasting

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32
Q

What are the random and fasting blood glucose levels of someone with hyperglycaemia?

A

Fasting >7mM

Random>11.1mM

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33
Q

What are the symptoms of hyperglycaemia?

A

Glucosuria (above renal threshold)
Polyuria (peeing lots)- osmosis
Polydipsia (XS thirst)- losing water

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34
Q

What is the effect on RBCs of hyperglycaemia?

A

Non-enzymatic glycosylation of haemoglobin- HbA1c

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35
Q

At what blood glucose level is someone considered hypoglycaemic?

A

<3mM

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36
Q

What are the symptoms of hypoglycaemia and what might these symptoms be mistaken as?

A 
Slurred speech
Reduced coordination
Dizziness/headache
Coma
Death

Initial symptoms are similar to drunkenness

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37
Q

Why can hypoglycaemia be fatal?

A

Glucose is essential for CNS function, without it CNS will starve and die

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38
Q

What are some possible causes of hyperammonaemia?

A
  1. High protein diet couple with a partial urea cycle defect
  2. Amino acid metabolism defect
  3. Re-feeding syndrome
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39
Q

How does re-feeding syndrome cause hyperammonaemia?

A

After long periods of starvation, there is depression of the urea cycle (as this is an induced cycle, up and down regulated by food). Reintroduction of food rapidly leads to excess amino acid degradation, there is insufficient urea cycle activity to dispose of the ammonia

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40
Q

What are the symptoms of the toxic effect of ammonia on the CNS?

A

Tremors
Slurred speech
Coma
Death

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41
Q

What is the effect of ammonia on the pH of the blood?

A

Increases it

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42
Q

How does hyperammonaemia lead to a reduction in energy supply?

A

The XS ammonia reacts with alpha-ketoglutarate which is a TCA cycle substrate
Lack of substrate inhibits the cycle therefore energy production is reduced

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43
Q

What is PKU?

A

Phenylketonuria- the presence of phenyl ketones in urine due to the defective enzyme: phenylalanine hydroxylase

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44
Q

What is the role of Phenylalanine hydroxylase?

A

Converts phenylalanine into tyrosine (which is converted into many neurotransmitters and other substances)

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45
Q

What is effect of a defective phenylalanine hydroxylase enzyme?

A

Build up of phenylalanine

Causes the driving of an alternative path to form phenylpyruvate

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46
Q

What are the consequences of PKU? (3)

A
  1. Mental retardation (phenylalanine inhibits brain development)
  2. Lack of neurotransmitter synthesis
  3. Phenylpyruvate prevents Pyruvate uptake into mitochondria- brain is starved of energy
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47
Q

How do you treat PKU?

A

Diet low in phenylalanine - Avoid high protein foods such a meat, eggs and milk

Need to ensure diet contains tyrosine as it is an essential amino acid

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48
Q

What are clincal symptoms of PKU?

A 
Severe interllectual disability
Developmental delay
Microcephaly 
Seizures
Hypopigmentation (because tyrosine can be used to make melanin)
49
Q

What is homocystinuria?

A

Defect in the CBS enzyme which leads to the build up homocysteine and methionine and homocystine in urine

50
Q

What is the pathophysiology of homocystinuria?

A
  1. Defective CBS enzyme which means homocysteine isn’t converted into cystathionine (and later cysteine). 2. This encourages the conversion of homocysteine to methionine.
  2. It also causes the oxidation of homocysteine to homocystine which is excreted in the ruin
  3. Build up of homocysteine and methionine and presence of homocystine in urine
  4. Homocysteine effects protein structure
  5. Methionine effects mental development
  6. No cysteine means there is little glutathione which leads to less protection against oxidative stress
51
Q

Why is homocystinuria initially confused with Marfan syndrome?

A

Because they both effect protein structure resulting in stretchy skin due to effect on connective tissue

There are similar clincal features such as lens dislocation and skeletal deformities

Both have associated CVS complications/diseases

52
Q

What is the defining feature of homocystinuria that differentiates it from Marfan’s syndrome?

A

There are neurological issues due to the high levels of methionine

53
Q

How do you treat Homocystinuria?

A

Low methionine diet

Vit B6 to increase remaining CBS activity

54
Q

What is the function of Chlyomicrons?

A

Transport diet fat from intestine to tissue (adipose)

55
Q

What is the function of VLDL?

A

Transit triacylglycerols made in liver to adipose tissue for storage

56
Q

What is the role of IDL?

A

Transport cholesterol synthesised in the liver to tissues

57
Q

What is the transport function of LDL?

A

Transport cholesterol synthesis in liver to tissues (like IDL)

58
Q

What is the transport role of HDL?

A

Transport excess tissue cholesterol to liver for disposal as bile salts and to cells requiring additional cholesterol

59
Q

Why would you get a high level of chylomicrons in the blood many hours after a meal if you have hyperlipidaemia?

A

Lack of breakdown due to lack of/insufficient/inactive lipoprotein lipase enzymes

60
Q

What is a symptom of hyperlipidaemia?

A

Abdominal pain

61
Q

What is the result of familial hypercholesterolaemia?

A

Increase LDL and cholesterol levels in blood due to absence or deficiency in LDL receptors

62
Q

What are some symptoms and consequences of familial hypercholesterolaemia?

A

Xanthelasma (yellowish deposit of fat underneath the skin, eg eyelids. While they are neither harmful nor painful, these minor growths may be disfiguring and can be removed)
Corneal arcus (rings around the cornea)
Increased atherosclerosis

63
Q

What enzyme is used to produce respiratory burst?

A

NADPH oxidase (transports electron across the membrane from NADPH to produce superoxide radicals)

64
Q

What deficiencies can cause increased oxidative stress?

A

G6PDH deficiency= reduced levels of NADPH:

  1. less reduction of GSSH back to GSH
  2. Less NADPH available for oxidative stress (NADPH oxidase)

SOD deficiency

Catalase deficiency

65
Q

What is pathophysiology of excessive alcohol intake?

A
  1. Uses NAD+ to convert alcohol to acetaldehyde and then to acetate, reducing the levels available for other process ie gluconeogenesis
  2. Leads to increased fatty acid synthesis- fatty liver
  3. Loss of enzymes
  4. GI disturbances (and chronic pancreatitis and potentially diabetes)
66
Q

How is NAPQI dealt with in the body and what are the consequences of that?

A

It is reacted with glutathione which depletes the body’s ROS defences

67
Q

What can be used to treat paracetamol overdoses and why does it work?

A

Acetylcysteine

Replenishes glutathione levels so liver can metabolism NAPQI and ROS defence is maintained

68
Q

Give a very basic description of atherosclerosis?

A
  1. Endothelial damage and dysfunction
  2. Foam cell formation
  3. Fatty streak
  4. Fibrous cap (around plaque)
  5. Plaque calcification and necrosis
69
Q

What are the 3 important signs of diabetes mellitus type 1?

A

Polyuria
Polydipsia
Unexplained weight loss

70
Q

What is something that is found in the urine of a type 1 diabetic?

A

Glucose

Ketone bodies

71
Q

What can untreated diabetes mellitus lead to? What are the symptoms of this?

A

Ketoacidosis

Hyperventilation 
Nausea
Vomiting
Abdominal pain 
Ultimately coma
72
Q

What are some complications of diabetes mellitus?

A 
Retinopathy
Atherosclerosis 
Infections 
Sexual dysfunction 
Miscarriages and still births
73
Q

What are the macrovascular complications of diabetes mellitus? (3)

A

MI
Stroke
Poor circulation to periphery

74
Q

What are the microvascular complications with diabetes mellitus? (4)

A

Neuropathy
Nephropathy
Retinopathy
Diabetic foot

75
Q

How can you monitor diabetes using RBCs?

A

HbA1c test

76
Q

What is diabetes insipidus?

A

A deficiency of ADH

Causing excessive thirst because you’re not saving your water

77
Q

What are the symptoms of diabetes insipidus?

A

Excessive thirst (polydipsia)
Polyuria
Signs of dehydration (headaches, dizziness)
Hypokalaemia (?)

78
Q

How can diabetes insipidus present in children?

A

Fever
Vomiting
Diarrhoea
May affect appetite, eating, weight gain and growth

79
Q

How does diabetes mellitus lead to ketoacidosis and what are symptoms of this?

A

Lack of insulin-mobilisation of fatty acids- increase in ketone body production (raises pH of blood/ smell acetone on breath)

Causes: hyperventilation, nausea, vomiting, dehydration-fluids needed, abdominal pain

80
Q

What is the role of leptin

A

Inhibits stimulatory neurones that increase appetite
Stimulates inhibitory neurones that decrease appetite

Works to decrease appetite

81
Q

What is Cushing’ syndrome?

A

Increased secretion of glucocorticoids from the zona fasciculata: cortisol

82
Q

What causes Cushing’s syndrome?

A

Prescribed glucocorticoids (most common)
Adrenal cushing’s: XS cortisol production by adrenal tumour
Cushing’s disease: benign pituitary adenoma secreting ACTH
Ectopic ATCH producing tumour: Non pituitary-adrenal tumour eg small cell lung cancer

83
Q

What are the symptoms of Cushing’s syndrome?

A 
Moon shaped face (lipogenesis)
Buffalo hump (redistribution of fat)
Abdominal obesity (redistribution of fat)
Purple striae (Proteolysis)
Easy bruising (proteolysis)
Acute weight gain
Hyperglycaemia causing polyuria and polydipsia 
Hypertension (cardiac hypertrophy)
Amenorrhagia
84
Q

What is cushing’s disease?

A

Cushing’s syndrome caused by a benign adenoma secreting ACTH in the pituitary

85
Q

What is Addison’s disease?

A

[opposite of cushing’s]

Decreased activity of adrenal cortex- lack of cortisol

86
Q

What causes Addison’s disease?

A

Autoimmune destruction of adrenal cortex

Pituitary/hypothalamic disorder leading to decreased ACTH or CRF release

87
Q

What are the signs and symptoms of Addison’s disease?

A 
Postural hypotension
Lethargy
Weight loss 
Anorexia
Increased skin pigmentation (increased MSH as consequences of increased POMC, this causes melanin synthesis) 
Hypoglycaemia
88
Q

What is an Addisonian crisis? What causes it?

A

Life threatening emergency due to adrenal insufficiency
Brought on by: severe stress, salt depravation, infection, trauma, cold exposure, over exertion, abrupt steroid withdrawal

89
Q

What are the symptoms of an addisonian crisis and how is it treated?

A 
Nausea 
Vomiting 
Pyrexia 
Hypotension
Vascular collapse

Treatment: fluid replacement and cortisol

90
Q

What is pheochromocytoma?

A

Chromaffin cell tumour- stimulates release of Noradrenaline

Characterised by severe hypertension, headaches, palpitation, diaphoresis (XS sweating), anxiety, weight loss, high blood glucose

91
Q

What is Conn’s syndrome?

A

Primary aldosteronism caused by hyperactivity of adrenal glands

Unilateral: adenoma
Bilateral: genetic

92
Q

What are the symptoms of Conn’s syndrome?

A

Hypertension
Muscle weakness and spasms
Tingling sensation
Xs urination

93
Q

How can you diagnose Conn’s?

A

Measure Renin

Would be released by kidneys but in this case it isn’t because there is increased BP and renal perfusion already. Renin levels will be lower than normal

94
Q

What is Grave’s disease? What is the most common cause?

A

Hyperthyroidism
Increase production and release of T3 and T4

Autoimmune disease producing antibodies that stimulate TSH receptors

95
Q

What are the symptoms of hyperthyroidism?

A 
Heat intolerance (increased BMR)
Weight loss
Hyperactivity 
Tachycardia 
Myopathy
(Goitre and bulging eyes)
96
Q

How do you treat graves disease?

A

Carbimazole

Thyroidectomy (if severe)

97
Q

What is the substance that can be used in the scanning of the thyroid gland?

A

Technetium 99m

98
Q

What is Hashimoto’s disease?

A

An autoimmune disease resulting in destruction of thyroid follicles leading to hypothyroidism

(More likely in women)

99
Q

What is the treatment for hashimoto’s disease?

A

Oral thyroxine (t4)

100
Q

What are the signs of Hashimoto’s disease?

A 
Cold intolerance (reduced BMR)
Weight gain
Tiredness, lethargy 
Bradycardia 
Goitre
Cretinism in children if undetected
Skin dry and flaky 
(Rarely:iodine deficiency)
101
Q

What does untreated hypothyroidism lead to in adults and children?

A

Adults: myxedema
Infants: cretinism

102
Q

Give the 3 main causes for anaemia?

A

Blood loss
Excess breakdown of RBCs
Deficient release of RBCs

103
Q

Why might you get Excessive breakdown of RBCs leading to anaemia?

A

Sickle cell anaemia

Thalassaemias: alpha and beta

104
Q

Why might you deficient release of RBCs leading to anaemia?

A

Poor haematopoiesis:
Iron deficiency anaemia
Megaloblastic anaemia: vitamin B12 and folate deficiencies

105
Q

What are the causes of an iron deficiency anaemia?

A 
Blood loss
Increased requirements 
Inadequate dietary supply 
Decreased absorption 
Anaemia of chronic disease (infections and malignancies)
Increased activity of macrophages
106
Q

What is thrombocythaemia?

A

Myeloproliferative neoplasm

Overproduction of platelets from megakaryocytes

107
Q

What is polycythaemia vera?

A

Myeloproliferative neoplasm
Overproduction of RBCs

Form of polycythaemia which is the increased volume percentage of haematocrit in blood

108
Q

What is myelofibrosis?

A

Myeloproliferative neoplasm

Haematopoietic tissue is replaced by connective tissue which can lead to pancytopenia

109
Q

What is polycythaemia? What are the two types?

A

Increased volume of haematocrit in blood

Absolute- increase of RBC
Relative - decrease in plasma

110
Q

What are the symptoms of polycythaemia vera?

A 
(Anything that comes from thicker blood)
Thrombosis 
Haemorrhages (GI tract and skin)
Burning pain in hands and feet
Pruritus (itchiness)
Gout 
Arthritis
Can lead to acute leukaemia or myelofibrosis
111
Q

What are good indicators of reduced spleen function?

A

Howell-Jolly bodies

112
Q

What are Howell- jolly bodies?

A

Histopathological findings of nuclear remnants (clusters of DNA) in circulating erythrocytes. During maturation in the bone marrow late erythroblasts normally expel their nuclei, but in some cases a small portion of DNA remains. Its presence usually signifies a damaged or absent spleen because a healthy spleen would normally filter this type of red blood cell

113
Q

What are the 3 possible causes for hypercalcaemia?

A
  1. Primary hyperparathyroidism: 1 gland develops adenoma which produces xs PTH which causes a break down of bone to raise Ca2+ serum levels (and decrease phosphate levels)
  2. Secondary hyperparathyroidism: vitamins D deficiency= low Ca2+ intake causing all 4 glands become hyperplastic and release even more (XS) PTH in an attempt to raise Ca2+ serum levels by breaking down bone
  3. Malignant hypercalcaemia: break down in bones, nothing to do with PTH levels (if anything they’re reduced), excessive Calcitriol/parathyroid hormone related peptide from cancers
114
Q

What are the symptoms of primary hyperparathyroidism?

A

Psychic Moans: tired, exhausted, depressed

Abdominal Groans: constipation, peptic ulcers, pancreatitis

Kidney Stones: kidney stones (+ polyuria)

Aching Bones: bone and muscle aches

115
Q

What are the causes of hypocalcaemia?

A

Vitamin D and calcium deficiency
Hypoparathryoidism (very rare)
Removal of parathyroid gland

116
Q

Calcium raised the threshold for nerve membrane depolarisation, therefore what is the effect of hyper/hypocalcaemia on neuronal activity and what are the related symptoms?

A

Hyper: leads to suppression: lethargy, confusion, coma

Hypo: leads to ‘excitable’ nerves: tingling, muscle tetany (cramping and spasms) and even epilepsy

117
Q

What can hypocalcaemia lead to?

A

Osteomalacia in adults : rickets in children

118
Q

What is gestational diabetes?

A

Diabetes brought on during pregnancy

119
Q

How does being pregnant cause diabetes?

A

Rate of insulin is increase and synthesis normally increases too. However in some cases the pancreas will fail to respond to demands and insufficient insulin is released. Loss of metabolic control leads to a rise in blood glucose and diabetes

MEH (Milly's) (39 decks)

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