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7- Weight Loss > Learning Objectives (NON-CLIC) > Flashcards

Learning Objectives (NON-CLIC) Flashcards

1
Q

What is the purpose of emesis?

Describe the physiological control of vomiting and gut motility

A

Defense mechanism

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2
Q

List different emetic stimuli.

Describe the physiological control of vomiting and gut motility

A
  • Blood
  • Intestine
  • Neural input from GI tract, labyrinth, and CNS
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3
Q

What are the two units that are make up the central neural regulation system of vomiting? And where are they located?

A

▪ Located in the Medulla
▪ The Vomiting (emetic) centre
▪ The Chemoreceptor Trigger Zone, (CTZ)

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4
Q

A) Describe the vomiting centre.

B) Describe the chemoreceptor trigger zone.

A

A)
▪ Collection of multiple sensory, motor and control nuclei
▪ Mainly in the medullary and pontile reticular formation
▪ Receives impulses from both vagal and sympathetic afferent nerves
▪ Responds to the incoming signals to coordinate emesis

B)
▪ Sensitive to chemical stimuli
▪ Main site of action of many emetic and antiemetic drugs (because CTZ is in an area where the BBB is relatively permeable
▪ Mediates motion sickness (due to various movements with the stimuli being the vestibular apparatus)

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5
Q

List the various stimuli of nausea vomiting.

A
  • Pain, repulsive sights and smells, and emotional factors travel from higher cortical centres to the vomiting centre
  • Stimulation of the sensory nerve endings in the stomach and duodenum through vagal afferents straight to CTZ
  • Or toxins/toxic chemicals which is sensed by enterochromaffin cells and released 5-HT up the vagal afferent nerves to CTZ then to vomiting centre
  • Disturbance of the vestibular apparatus (e.g. motion sickness) where stimuli from labyrinth -> vestibular nuclei -> CTZ -> vomiting centre)
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6
Q

Describe the stages of vomiting.

A
  1. Nausea - feeling of wanting to vomit, associated with autonomic effects like salivation/pallor/sweating
    1. Retching - strong voluntary effort to vomit with no actual vomiting (unproductive)
    2. Vomiting - Expulsion of gastric contents thought the mouth
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7
Q

What type of vomiting do esophageal varices and peptic ulcer cause?

A

▪ Hematemesis - vomiting fresh blood or altered blood (altered = ‘ground coffee’ look as they are further down in the GI tract and hence the blood has gone some changes on the way, can be indicative of a serious bleed)

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8
Q

Other than hematemesis, name two other types of vomiting. Provide examples of underlying causes of each.

A

▪ Projectile vomiting - example: gastric outlet or upper GI obstruction
▪ Early-morning vomiting - examples: pregnancy, alcohol dependency, metabolic disorder (E.g. uremia)

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9
Q

What are two factors that need to be considered when prescribing anti-emetics?

A

▪ Cause of vomiting must be known to prescribe (better to treat the cause of the vomiting if possible)
▪ Drug must be chosen based on where it acts, and the source of the stimuli

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10
Q

A pregnant woman with hyperemesis gravidarum requires management. What are some of the considerations when using anti-emetics in pregnancy?

A

▪ Benefit: Risk ratio (to mother and fetus)

▪ Try and avoid giving any in the first trimester if possible

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11
Q

List 4 types of anti-emetic medications based on their mechanism of action. (Most commonly used in primary and secondary care)

A

▪ Antimuscarinics (M1)
▪ Antihistamines (H1)
▪ Dopamine antagonists (D2)
▪ 5HT3 Antagonists

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12
Q

One type of antiemetics is antimuscarinic drugs.

A) Name the location of muscarinic receptors where these drugs will act.

B) Name an example of an antimuscarinic anti-emetic drug.

C) Name a common presentation that the example in (B) usually used for in primary care.

D) Name 4 side effects of antimuscarinic drugs.

A

A) Vestibular nuclei which receives impulses from the inner ear

B) Hyoscine Hydrobromide (caution in epilepsy)

C) Motion sickness (available in tablets or patches)

D) Dry mouth, blurred vision, hot/flushed skin, bradycardia followed by tachycardia

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13
Q

Another type of antiemetics are antihistamines (H1 Receptors antagonists).

A) State the situations in which these are most useful.

B) List some of the side effects of antihistamine medications.

C) Provide 3 examples of antihistamine antiemetic medications.

A

A) Good for numerous causes of N/V. Especially if someone has a generic type not associated with a specific diagnosis: including motion sickness + stomach irritants

B) Drowsiness, antimuscarinic effects

C)
• Cinnarizine (Particularly good for vestibular disorders and motion sickness rather than generic N/V , contraindicated in acute prophyria, SE: drowsiness, Nausea, weight gain)
• Cyclizine (Generic N/V, motion sickness, vestibular disorders, and good for palliative care, contra in severe liver disease, SE’s: Angle closure glaucoma, depression, drowsiness)
• Promethazine (N+V, motion sickness, labyrinthine disorder and particularly goo din severe morning sickness, contra in under 2yo, SE’s: drowsiness, anxiety, dry mouth)

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14
Q

Another type of antiemetic medications are dopamine antagonists. List three examples of dopamine antagonists, with brief description of indications, contraindications and SE examples.

A

Examples:

  • Phenothiazines - mainly with severe N+V related to cancer radiation therapy (E.g prochlorperazine)
  • Domperidone - N + V associated with cytotoxic causes and GI causes
  • Metoclopramide - N + V, N + V associated with migrane/ehcmo, radio t

(For details on the rest check lecture LO 1 Week 7)

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15
Q

One type of antiemetics is 5HT3 antagonists drugs.

A) Name the location of receptors where these drugs will act.

B) Name an example of 5HT3 anti-emetic drug.

C) Name a common presentation that the example in (B) usually used for in primary care.

D) Name side effects of these drugs.
A

A) Prime site of action is CTZ

B) Ondansetron (contraindicated in long qt syndrome) - drugs generally end with ansetron

C) Particularly useful in managing N/V in patients receiving cytotoxic, radiation therapy and in post operative N/V

D) Can get headaches and GI upsets but generally uncommon

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16
Q

A) Describe the neuronal control of GI tract.

B) Describe the hormonal control of the GI tract.

A

A)
▪ Parasympathetic nerves increase activity of enteric nervous system (increase smooth muscle tone, promote sphincter relaxation)
▪ Sympathetic Inhibits the activity
▪ There are two plexuses which are controlled by parasympathetic and sympathetic nerves:
○ Myenteric plexus (out plexus) - increased tone of gut wall, increase strength of contraction, increase rate of contractions, inhibits pyloric, ile1
○ Submucosal plexus (inner plexus)

B)
▪ GI hormones exert effects of target cells: secretin, gastrin, cholecystokinin, somatostatin

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17
Q

List the different types of laxatives.

A
  • Bulk-forming laxatives (Bulk-fibre provides increased volume and promotes peristalsis by distention)
  • Stimulant laxatives
  • Faecal softeners (coats and breaks up particles)
  • Osmotic laxatives (draw water out, liquid mixes with stool to soften)
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18
Q

Name a Bulk-forming laxative.

A

Ispaghula husk

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19
Q

Name a stimulant laxative.

A

Senna (not good if someone has cramps already)

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20
Q

Name a softner laxative.

A

Docusate (for chronic constipation)

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21
Q

Name a osmotic laxative.

A

Lactulose

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22
Q

What is the basic pathophysiology of diarrhoea.

A

Diarrhoea involves both an increase in the motility of the GI tract and a decrease in the absorption of fluid and thus a loss of electrolyte.

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23
Q

Describe the approach to the treatment of acute diarrhea.

A
  1. Maintenance of fluid and electrolyte balance e.g. oral rehydration preparation
  2. Antimotility drugs (Loperamide ie imodium)
  3. Antispasmodics (reduce smooth muscle tone) e.g. hyoscine butylbromide (buscopan), mebeverine
  4. Occasionally antibacterial agent is indicated e.g. systemic bacterial infection, campylobacter enteritis, shigellosis and salmonellosis
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24
Q

A) What is Buscopan?

B) What is it used for?

A

A) Anti-Muscarinic, relaxes intestinal spasm (its called hyoscine butyl-bromide)

B) GI/GU spasms, irritable bowel and acute diarrhoea, and acute spasms + palliative care for excess respiratory secretions)

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25
Q

What drugs do you use for chronic diarrhea?

A
  • Anti-motility agents (inhibit peristalsis)

- Bulk forming drugs (conversely used in controlling diarrhoea associate with diverticular disease)

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26
Q

A) Name an anti motility agent

B) Describe its MOA.

A

A) Loperamide (Imodium)

B) Works by slowing gut motility and affecting water and electrolyte movement through the gut - acts on opioid receptors in the gut.

(good for acute and chronic diarrhoea, and faecal incontinence)

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27
Q

What is the difference between alternative and complimentary medicine?

A

Alternative = use of complementary and alternative medicine in place of conventional medicine

Complementary = use of CAM together with conventional medicine

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28
Q

What is meant by medical pluralism?

A

Adoption of more than one medical system (beliefs/behaviours/treatments)

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29
Q

List popular complementary and alternative medicine modalities.

A
  • Homeopathy
  • Herbal Medicines
  • Osteopathy and chiropractic
  • Acupuncture
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30
Q

Briefly describe how homeopathic preparation.

A
  • Principle of similars (a substance that causes the disease in a healthy person can cure the disease in an unhealthy person.
    • Preparations must undergo potentisation which involves serial dilutions of a mother tincture in succession (Commonly given at 30C dilution = 1 in 10030)

No direct harm or interactions

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31
Q

What important information regarding the use of St John’s Wort (Hypericum) should you give a patient who is asking for advice about herbal medicines.

A

▪ It interacts with other drugs - hormonal contraceptives, anti-depressives, anti-coagulants, anti-epilepsy agents, anti-cancer agents

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32
Q

Provide three potential ‘direct harms’ caused by herbal medicines.

A

▪ Adverse drugs reactions
▪ Drug interactions
▪ Quality control (?)

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33
Q

List four potential direct harms from chiropractic and osteopathy.

A

▪ 50% of chiropractic patients suffer an adverse reaction
▪ Tearing of artery wall leading to stroke
▪ Injury to spinal cord
▪ Chiropractic X Ray

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34
Q

Give two examples of potential direct harm of acupuncture.

A

▪ Infections

▪ Pneumothorax

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35
Q

A) What is PTSD?

B) List 5 risk factors for PTSD.

C) List symptoms associated with PTSD.

A

A) An anxiety disorder associated with experiencing or witnessing single, repeated or multiple events.

B)
▪ Exposure to traumatic event
▪ Severity of incident - the more severe and the greater the perceived threat to life, also intentional harm appears to be more likely to cause PTSD than natural disasters 
▪ Female sex
▪ Younger Age
History of mental health disorder

C)
▪ Re-experiencing (intrusive memories) - thoughts, images, flashbacks, nightmares
▪ Avoidance - of anything related to the event (E.g people, places, feelings)
▪ Hyperarousal -
▪ Negative alterations in mood and thinking
▪ Emotional Numbing
▪ Dissociation
▪ Interpersonal difficulties or problems with relationships

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36
Q

What is the treatment/management of PTSD?

A

▪ Trauma-focused cognitive behavioural therapy (Exposure therapy where they are exposed to traumatic memories and recall them + Cognitive therapy where any misrepresentation and overestimated threat by a person is identified so they think differently)
▪ Eye movement desensitisation and reprocessing - Making eye movements while recaling events helping people process the events as usually PTSD is from incompletely processed traumatic events - found to reduce symptoms
• Consider for those 1-3 months after non-combat-related event
• Offer to those presenting more than 3 months after non-combat-related

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37
Q

True or False. One effective and safe way of managing, and in this case preventing, PTSD in adults is psychological debriefing.

A

▪ False - this can increase risk of the disorder as it may cause secondary traumatisation, and prevent potentially protective response of denial and distancing.
▪ NICE Guidelines say that it should not be offered

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38
Q

List some of the advantages and disadvantages of classifying mental disorders.

A

Adv:

  • Standardise diagnosis and treatment
  • Guides research

Dis:

  • Lack of ‘zone of rarity’ between health and disease when classifying mental disorders - hiatus between features of disease in biological disorder allow you to distinguish clearly between diseases
  • Risk of misdiagnosis and over treatment
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39
Q

Define weight loss.

A

loss of 5% over 6 months

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40
Q

What are psychosocial causes of weight loss?

A
  • Depression
  • Bereavement
  • Eating disorders
  • Substance misuse
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41
Q

What are gastrointestinal causes of weight loss?

A
  • Oral problems
  • Malabsorption
  • Malignancy
  • IBD
  • Liver disease (e.g. cirrhosis makes it more difficult for the body to process nutrients)
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42
Q

What are endocrine causes of weight loss?

A
  • Diabetes
  • Hyperthyroidism
  • Addison’s disease (causes decreased appetite)
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43
Q

Name a cardiac cause of weight loss?

A

Heart failure

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44
Q

Name a respiratory cause of weight loss.

A

COPD

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45
Q

Name a renal cause of weight loss.

A

advanced CKD

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46
Q

What are inflammatory causes of weight loss?

A
  • Vasculitis (tx causes lack of appetite and due to loss of muscle cachexia)
  • SLE
47
Q

How can medication be related to weight loss?

A
  • Prescribed medications like anti-cancer, metformin, and SSRI’s
  • Herbal Medicines
  • Drugs misuse
48
Q

List causes of increased appetite with weight loss.

A
  • Thyrotoxicosis
  • poorly controlled diabetes
  • Malabsorption
49
Q

List possible investigations for weight loss.

A 
Possible Investigations:
▪ Urine 
	• Diabetes
	• Renal disease
	• Haematuria
	• Bence-Jones protein
▪ Blood tests 
	• FBC
	• LFT
	• RENAL FUNCTION/ELECTROLYTES
	• GLUCOSE/HBA1C
	• TFT
	• CRP/ESR
	• CALCIUM
▪ CXR
▪ Faecal occult blood (blood in faeces that is not visibly apparent)
▪ CT Imaging
▪ Referral for endoscopic Investigation
50
Q

How does graves disease present?

A
  • Weight loss
  • Tearful
  • Anxious
  • No loss of appetite but eating more if anything
  • enlarge gland
51
Q

How may addison’s disease present?

A
  • Tiredness
  • Pigmentation of the skin (buccal mucosa, palm of hand and other parts of the body)
  • weight loss
  • Carry a short syncachten test
52
Q

If there was weight loss then stabilised and no more what would you do?

A

Monitor and see how things go!

53
Q

What is the estimate of the number of people in the UK with eating disorders?

A

1.25 million

54
Q

What group, in terms of gender and age, is at most risk of eating disorder?

A

Girls and young women aged 12-20

55
Q

What age range do 95% of eating disorders present in?

A

12-25 year old

56
Q

Name three biological factors that increase risk of eating disorders.

A

▪ Gender (Female)
▪ Genetics (concordance: mono>dizygotic twins + someone with a mother or sister who has had anorexia)
Co-morbidities (Depression, anxiety, OCD)

57
Q

Name three Psychological Factors that increase risk of eating disorders.

A

▪ Low self esteem
▪ Poor coping mechanisms
▪ Personality traits e.g perfectionist, obsessive thinking

58
Q

In the context of family history, give an example of a psychological factors that make contribute to a patient with anorexia.

A

Family with high perfectionistic obsessive traits

59
Q

Give an example of a psychological factor that may contribute to a patient with Bulimia or binging.

A

▪ Family with obesity, depression, substance abuse

60
Q

Describe the management of Anorexia nervosa.

A

1- FBT (Family Behavioural Therapy) - aim of this is to feed the child, as they are unable to make decision regarding their own health when they are in an underfed state. Encouraging the adults to take back control of the child’s eating habits
2- Motivation - help child see negatives (tiredness, agitation etc..) and the positives of weight gain (more energy, clear headedness)
Medication - here food is medicine! You prescribe food! Decision is whether, orally, supplement drink, or naso-gastric tube. (little evidence for psychoactive medications, important to avoid QTc prolongation - some evidence for olanzapine antipsychotic to help with rumination and aid weight gain in AN)
4- Admission only if physical health is severely compromised

61
Q

A) Describe the classification of Anorexia Nervosa in DSM-5.

B) List clinical features of Anorexia Nervosa.

A

A) a. Restriction of energy intake relative to requirements leading to low body weight (Significant Weight Loss)

	a. Significantly Low body weight = at least 15 % below that expected 
b. Intense fear of becoming fat or gaining weight (Fear of being fat)
c. Disturbance in the way ones body weight or shape is experienced (persistent lack of recognition of the seriousness of current low body weight) (body image distortion)
d. (ICD Has amenorrhoea and loss of sexual interest as extra criteria) 
B)
- Excessive weight loss
- Fatigue
- Amenorrhoea
- Lanugo hair is fine, soft hair across most of the body
- Hypokalaemia
- Hypotension
- Hypothermia
- Changes in mood, anxiety and depression
Solitude
62
Q

List the complications associated with Anorexia Nervosa.

A
  • Cardiovascular complications: include arrhythmia, cardiac atrophy and sudden cardiac death, Refeeding syndrome, mitral valve prolapse
  • Haematological: Thrombocytopenia, Decreased sedimentation rate, pancytopenia due to starvation
  • Pulmonary:
    Respiratory failure, aspiration pneumonia, spontaneous pneumothorax, emphysema
63
Q

A) Describe one significant risk associated with rapid refeeding of a malnourished patient.

B) List risk factors.

A

▪ Refeeding Syndrome (occurs when someone is in severe nutritional deficit for an extended period of time.)
▪ Potentially fatal shift in electrolytes and fluids
▪ Complications = hypophosphatemia, hypomagnesemia, hypokalaemia, cardiac failure, coma, death
▪ Signs = bradycardia, hypotension, delirium, oedema

64
Q

A) Describe the classification of Bulimia Nervosa in DSM-5.

B) List clinical features of bulimia nervosa.

A

A) a. Recurrent episodes of binge eating (1- eating more than what ordinary people would eat in similar circumstances, 2- lack of control during the episode)

b. Recurrent inappropriate compensatory behaviours to prevent weight gain (purging - e.g. use laxatives, induce vomiting to prevent calories being absorbed)
c. A and B occur on average once a week for 3 months
d. Self-evaluation is unduly influenced by body shape and weight
e. The behaviour does not occur exclusively during episodes of AN

B)

  • Usually teenager girl normal weight
  • Alkalosis, due to vomiting hydrochloric acid from the stomach
  • Hypokalaemia
  • Erosion of teeth
  • Swollen salivary glands
  • Mouth ulcers
  • Gastro-oesophageal reflux and irritation
  • Calluses on the knuckles where they have been scraped across the teeth. This is called Russell’s sign.
65
Q

A) Describe one significant risk associated with rapid refeeding of a malnourished patient.

B) List risk factors.

A

▪ Refeeding Syndrome (occurs when someone is in severe nutritional deficit for an extended period of time.)
▪ Potentially fatal shift in electrolytes and fluids as cells slow metabolism during starvation then when they begin to process glucose, protein and fats again they use up all the electrolytes below
▪ Complications = hypophosphatemia, hypomagnesemia, hypokalaemia, cardiac failure, coma, death
▪ Signs = bradycardia, hypotension, delirium, oedema (causes heart failure and potential fatal arrhythmias)

B)

  • Low BMI (lower than 20 - low height or low weight)
  • Had little to eat for the last 5 days
  • Weight loss of over 15% in the last three months

(management is through slow feeding, monitoring electrolytes, fluid balance monitoring, ECG, and giving them vitamins)

66
Q

What is the normal range of sodium levels?

A

135-145mmol/L

67
Q

Define Hyponatremia (occurs in 15-20% of all hospital admissions)

A

▪ Mild: 130 -135mmol
▪ Moderate: 125-129mmol
▪ Severe: <124mmol

68
Q

What is the difference between acute and chronic Hyponatremia?

A

▪ Acute = <48 hours

Chronic = >48 hours

69
Q

Describe what happens when there is an acute onset of hyponatremia.

A

▪ Plasma osmolality falls quickly

– Water rapidly flows into cerebral cells causing swelling

70
Q

Describe the Pathophysiology of Hyponatremia.

A

More water relative to sodium

71
Q

Clinical Features of hyponatremia. (these depend on whether it is acute or chronic)

A

Maybe None
Nausea, Confusion, Headache
Coma, Seizures, Vomiting

72
Q

Causes of hypo and hyper should be thought of in the context of fluid status:

A

▪ Hypovolaemia
• Pathophysiology: deficient in water and Na, however more water than Na in blood due to excess sodium loss
• Cause Examples: Renal Diuretics, adrenocortical failure, vomiting, diarrhea, burns

▪ Euvolaemia
• Pathophysiology: Normal Na, Excess water (so they are clinically not overloaded or underloaded)
• Cause Examples: Polydipsia, Iatrogenic (IV Fluids), Syndrome of Inappropriate Antidiuretic Hormones (SIADH)

▪ Hypervolaemia
• Pathophysiology: Water and Na retention
• Cause Examples: Heart failure, cirrhosis, CKD

73
Q

Describe the MoA of ADH. (Also called vasopressin)

A

▪ Produced by the hypothalamus
▪ Stored in the posterior pituitary
▪ Acts on the distal tubule and collecting ducts
▪ Increases systemic vascular resistance (increase BP) and increases water reabsorption in the kidneys (promotes water reabsorption)

(ADH = allows the production of aquaporins channels on the apical membrane of principal cells in the nephron tubule which allows the reabsorption of water)

74
Q

What stimulates the release of ADH?

A

▪ Hyperosmolality

- Decreased Atrial receptor firing (hypovolemia)

75
Q

A) Describe the pathophysiology of SIADH.

B) List potential causes.

A

A) Excessive water retention caused by ADH without a physiological cause resulting in hyponatremia (diagnosis by exclusion)

B) 
▪ Idiopathic 
- Tumors
▪ CNS
▪ Lung problems (pneumonia)
▪ Drugs
76
Q

Describe the investigations (diagnostic algorithm) of hyponatremia. (take home message from the graph below)

A
  1. Electrolyte, Glucose, biochemistry
    1. Plasma Osmolality
    2. Urine Osmolality
      Maybe Urine Sodium
77
Q

Describe the difference in the management of acute and chronic hyponatremia.

A

▪ Acute = rapid fall in plasma osmolality = water rapidly flows into cerebral cells causing swelling
▪ Acute onset with signs of cerebral oedema = prompt correction with hypertonic saline
▪ Chronic = gradual development = allows cerebral cells to reduce intracellular osmolality = osmotic gradient forcing is reduced
▪ Chronic onset = rapid overcorrection can be dangerous = so slow correction is key (<10mmol/L/24hr) (if rapid administration of sodium, fluid would flow from cerebral cells to ECF rapidly and damage cells)

78
Q

Describe the difference in management of hypovolemia, euvolemia, and hypervolemia in hyponaturaemia/

A

▪ Hypo = you correct this. (For example, if they are on diuretics, you stop then then you give fluids as you need to correct the hypovolemia)
▪ Euvo and Hypervolemia = fluid restriction

79
Q

Define Hypernatraemia.

A

▪ Na >145

▪ Severe = >160mmol/L

80
Q

Describe in simple terms the pathophysiology of hypernatraemia. And give three examples of pathophysiology causes.

A

▪ Deficit of water relative to sodium
▪ Examples:
• Free water loss
• Inadequate water intake (limited access to water)
• Excess Na (rarely) - due to excessive salt intake (orally, IV)

81
Q

Provide examples of why a patient may experience free water loss leading to hypernatraemia.

A

▪ Renal: osmotic diuretic
▪ GI: diarrhea
▪ Skin: Sweating
▪ Diabetes Insipidus (lack of Vasopressin/ADH or ADH that doesn’t work - cannot make concentrated urine, too much water loss) - this is a condition where there is polyuria and polydipsia without diabetes

82
Q

What is cranial diabetes insipidus?

A

Lack of ADH from hypothalamus

83
Q

Describe the management of hypernatraemia.

A

▪ Depends on the cause
▪ Oral fluids
▪ IV fluids with caution
▪ Treatment of diabetes insipidus (just be aware of this you don’t need to know the treatment)

84
Q

What is the normal potassium range?

A

3.5-5.5mmol/L

85
Q

Define hyperkalaemia..

A

Mild - 5.5-5.9
Moderate - 6.0-6.4
Severe - >6.5

86
Q

Describe the symptoms of Mild to moderate high K.

A

Asymptomatic

87
Q

Describe the symptoms of severely high hyperkalemia.

A

▪ Can cause muscle weakness

▪ Or remain asymptomatic until collapse/arrest

88
Q

What is the main investigation test in suspected hyperkalemia? Further, describe the findings that may be revealed by this investigation.

A

▪ Investigation: ECG

▪ Findings: Tall/Big T wave, prolonged PR interval, Wide QRS Complex

89
Q

Other than ECG, what other investigations can you carry out in suspected hyperkalemia.

A

▪ Creatinine/eGFR, Sodium, bicarbonate

90
Q

List three potential causes of pathophysiology underlying hyperkalemia.

A

▪ Excessive intake
▪ Inadequate excretion
▪ Redistribution

91
Q

Name two examples of underlying causes that may lead to excessive intake of potassium leading to hyperkalemia.

A

▪ Dietary potassium (usually only problem when there is reduced excretion)
▪ IV Fluids

92
Q

Inadequate excretion of potassium can lead to hyperkalemia. One of the causes if reduced aldosterone.

A) Name three medications that lead to reduced aldosterone

B) Name a hormonal condition that can lead to reduced aldosterone.
A

A)

  • ACEi
  • ARBs
  • Spironolactone

B) Addison’s disease

93
Q

Aside from reduced aldosterone, provide 3 more examples of inadequate excretion of potassium leading to hyperkalaemia.

A
  1. Reduced GFR - AKI/CKD
    1. Renin-inhibition - NSAIDS/BETABLOCKERS
    2. Tubulo-interstitial disease (usually caused by diabetes)
94
Q

A) What sort of electrolyte imbalance can acidosis cause? Describe the pathophysiology.

B) Name three examples that can cause redistribution of potassium around the body, and as such lead to hyperkalaemia.

A

A)
▪ Hyperkalemia
▪ By redistribution of potassium

B)
▪ Insulin deficiency
▪ Rhabdomyolysis
▪ Tumor Lysis Syndrome

95
Q

Describe the management of Hyperkalemia, including medications used.

A

1- Stabilize cardiac membrane - IV Calcium Gluconate
2- Shift K into cells (here is doesn’t become dangerous) - salbutamol, Insulin/dextrose (dextrose is given as insulin will reduce blood sugar), bicarbonate
3- Remove K from body - ion-exchange resin (PR/PO), Dialysis

96
Q

Define hypokalaemia.

A

<3.5mmol/L

3-3.4 - asymptomatic

<2.5 = severe = muscle weakness, tiredness, paralytic ileus

97
Q

List the three potential pathophysiology mechanisms that could lead to hypokalemia.

A

▪ Excessive Loss
▪ Inadequate Intake
▪ Redistribution

98
Q

List causes of hypokalaemia due to:

  • Excessive loss
  • Inadequate intake
  • Redistibution
A

1- Excessive loss:

  • Urine loss
  • Mineralocorticoid excess - conns syndrome (aldosteronism)
  • Diuretic (loop/thiazide)
  • GI (vomiting, NG aspiration, diarrhoea, laxative abuse)

2- Inadequate intake

  • dietary deficiency
  • IV Fluids

3- Redistribution :

  • Alkalosis
  • Insulin
  • Beta agonists (salbutamol)
99
Q

Describe Investigations of hypokalemia.

A

▪ Blood tests - biocarbonate, magnesium, calcium
▪ Renin
▪ Urinary Potassium
▪ ECG = ST depression, T Wave Inversion, prominent U waves, Long QU interval

100
Q

Describe the management of hypokalemia.

A
  • KCl Orally

- IV- Higher concentrations should be given centrally

101
Q

What is normal calcium levels in the blood?

A

2.1-2.6mmol/l

102
Q

What do you have to keep in mind if someone’s blood results show hypercalcaemia prior to taking management steps?

A

when there is hypercalcemia, it is important to view the albumin levels as calcium binds to the albumin, and there might be a case of hypoalbuminemia, so the calcium levels are actually normal) Adjusted calcium = total calcium - 0.02 (40-albumin) - just bare in mind)

103
Q

A) List the clinical features of hypercalcaemia.

B) List the causes of hypercalcaemia.

A 
A)
Clinical features:
	• Bones: musculoskeletal pain/Bone pain
	• MOANS: depression
	• GROANS: abdominal pain
	• STONES: renal colic
Can present acutely with sever hypercalcemia and dehydration

B) ▪ Normal or High PTH
• Primary hyperparathyroidism
• Tertiary Hyperparathyroidism
▪ If Low PTH levels (then the causes would be…):
• Malignancy (lung, breast, renal, lymphoma, myeloma)
• Elevated 1,25-dihydroxyvitamin D (this is the activated form of vitamin D as it is firstly not active and requires activating by the kidney - consider Vitamin D supplements or some medications that have this active form in them and consider Sarcoidosis as the lesions that are formed release this 1,25 dihydroxyvitamin D - not known why this happens)
• Milk-alkali syndrome (Rare) people that take too much rennie or gaviscon as they contain calcium
• Thiazide diuretic
• Lithium

104
Q

What is sarcoidosis?

A

A rare condition that causes small patches of red and swollen tissue, called granulomas, to develop in the organs of the body. It usually affects the lungs and skin.

Clinical Features:

  • Skin lesions (red-brown macules and papules usually affecting the face)
  • SOB
  • Persistent cough
105
Q

A) Describe the investigations of hypercalcaemia.

B) Describe management of hypercalcaemia

A

A)
Investigations:
▪ PTH LEVELS!
▪ Bone Profile: calcium, magnesium, Phosphate (helpful) (phosphate and calcium have an inverse relationship)
▪ Renal Function (tertiary hyperparathyroidism)
Screen for malignancy - CXR, MYELOMA SCREN, CT

B)
Management:

Treat underlying cause
Requires urgent management

106
Q

A) Describe the clinical features of hypocalcaemia.

B) Describe the causes.

C) Describe management of hypocalcaemia.

A

A)
Clinical Features:

Mild = asymptomatic
Severe = muscle spasms and tetany

Signs:
▪ Trousseau’s Sign (you put a blood pressure cuff, and inflate it, you should see flexion of the risk and MCP joints)
▪ Chvostek’s Sign (tapping the facial nerve leading to abnormal stimulation with lip twitching or all facial muscles spasm)

B)
Causes:
▪ Chronic Kidney Failure
▪ Hypoparathyroidism (common cause is accidental injury/removal during thyroidectomy)
▪ Pseudohypoparathyroidism (genetic condition where the body fails to respond to PTH)
Hypomagnesaemia

C)
Management:
Depends on causeEmergency treatment of hypercalcemia = IV Calcium gluconate

107
Q

Define Hypo and hyper magnesaemia.

A 
Hypo = <0.75mmol/L 
Hyper = >1.0mmol/L
108
Q

a) What are the clinical features of hypomagnesaemia.

B) List causes.

C) Investigations?

D) Management?

A

A) Mild = asymptomatic
Severe = tetany

B) Cause:
Inadequate intake EtOH excess (alcohol misuse), malnutritionExcessive loss - urinary / GIOther - PPI, pancreatitis

c)ECG

D)

  • Tx underlying cause
  • IV Mg (oral is limited use)
109
Q

A) What are the clinical features of hypermagnesaemia.

B) List causes.

C) Investigations?

D) Management?

A

A) Clinical features:

- Bradycardia
- Hypotension

B) Causes:Magnesium containing medications

C) ECG

D) Promote renal excretion

110
Q

Define hypo and hyper phosphataemia.

A 
Hypo = <0.8mmol/L
Hyper = >1.4mmol/L
111
Q

A) What are the clinical features of hypophosphataemia.

B) List causes.

C) Management?

A

A) wide ranging

B)
Redistribution into cells - refeeding syndrome
Inadequate intake - Malnutrition
Increased Excretion - Primary parathyroidism

C)

  • Oral supplementation
  • IV in critical care
112
Q

A) What are the clinical features of hyperphosphataemia.

B) List causes.

C) Management?

A

A)
Pruritis
Long term calcium and phosphate deposition

B) AKI
CKD

C)
Dietary restriction
Phosphate binding drugs

113
Q

A patient is required to be detained under the Mental Health Act 2003, and a NG tube is used due to their condition of Anorexia Nervosa. List the hazards that are associated with this type of feeding in this patient.

A
  • Misplaced tubes
  • Re-feeding syndrome (hypophosphotaemia - Confusion, hesitation, seizures, muscle breakdown)
  • Electrolyte imbalance
  • Constipation

7- Weight Loss (1 decks)

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