1
Q
list possible physical causes of weight loss
A
thyroid disorders
diabetes
consideration of malignancy
gastro-intestinal disorders
2
Q
what is the HEADSS assessment?
A
review of ‘systems’ for adolescents since they have few physical health problems, medical issues come from risky behaviours. ask about the context of a teens life…
Home Education Activities/Employment Drugs Suicidality Sex
3
Q
what questions would help in a suspected eating disorder consultation
A
do you think you need to lose weight? have you ever made yourself sick, given yourself diarrhoea or taken diet pills? how do you feel in general? Hx of cough? altered bowel habits? urinary symptoms? sweats or excessive thirst? dizziness? ask about periods? do you think you have a problem with your eating?
4
Q
what is the PHQ-9 modified for adolescents score used for?
A
the severity measure for depression - age 11-17.
5
Q
what is lanugo hair?
A
fine soft hair. a symptom of deep starvation
6
Q
what clinical signs might you see if a pt had bulimia nervosa?
A
signs of repeated vomiting such as discoloured teeth and Russells sign on the hands
there may be no obvious stigmata of the disease on examination and pt’s often have a normal BMI, is may not present with weight loss
7
Q
what history would suggest anorexia nervosa?
A
deliberately losing weight, probably for a sustained period and restricting diet and over-exercising. physical changes such as fatigue and loss of periods
8
Q
what would be the next appropriate investigation after suspicion of anorexia nervosa during history?
A
ECG and bloods
9
Q
what are the potential dangerous effects of anorexia?
A
CV:
- mitral valve prolapse
- sudden death-arrhythmia
- bradycardia and hypotension
- refeeding syndrome
Haematological: - pancytopenia due to starvation - thrombocytopenia - decreased sedimentation rate (dampens down bone marrow)
pulmonary:
- respiratory failure
- spontaneous pneumothorax
- emphysema
- aspiration pneumonia
endocrine and metabolic:
- amenorrhoea
- infertility
- osteoperosis
- thyroid abnormalities
- hypercortisolaemia
- arrested growth
- neurogenic diabetes insipidus
- hypoglycaemia
neurological:
- cerebral atrophy
opthalmic and dermatological:
- starvation associated pruritus
- languo haor
- alopecia
- dry skin
- lagophthalmos
GIT:
- constipation
- re-feed pancreatitis
- acute gastric dilation
- delayed gastric emptying
- hepatitis
- dysphagia
10
Q
what would be the next referral for someone with anorexia?
A
child and adolescent mental health service
11
Q
what are some of the potential hazards of nasogastric feeding in a pt with AN?
A
misplaced tubes
re-feeding syndrome
electrolyte imbalance
constipation
12
Q
what is the purpose of emesis?
A
a defence mechanism
13
Q
list different emetic stimuli
A
- blood
- intestine
- neuronal input from GI tract, labyrinth and CNS
14
Q
what are the 2 units that make up the central neural regulation system of vomiting? and where are they located?
A
- the vomiting centre
- collection of sensory, motor and control nuclei
- receives input from vagal and sympathetic afferent nerves
- responds to incoming signals to coordinate emesis - the chemoreceptor trigger zone
- sensitive to chemical stimuli
- main site of action of many emetic and antiemetic drugs (BBB relatively permeable)
- located in the medulla and pontine reticular formation
15
Q
what area is concerned with the mediation of motion sickness? describe the stages of motion sickness
A
chemoreceptor trigger zone (CTZ)
signals from LABYRINTH (inner ear) -> VESTIBULAR NUCLI -> CTZ-> VOMITING CENTRE -> VOMIT
16
Q
list the main neurotransmitters involved in passing on the messages, and in the emesis/ anti-emesis process
A
Ach Histamine 5-HT Dopamine Substance P
(receptors found in relevant areas)
17
Q
demonstrate how the various pathways in the control of vomiting are linked
A
- higher cortical centres (pain, repulsive sights, smells and emotions)
- vagal afferents, [direct] (convey signals from gut from enterochromaffin cells)
- and the CTZ (main site for sensing emetic stimuli)
- -> feed into the vomiting centre (integrates incoming signals: coordinates emesis)
- vestibular nucliei (inout from the labyrinth)
- vagal afferents (convey signals from the gut to brainstem)
- -> feed into the CTZ (main site for sensing emetic stimuli) –> vomitting centre (integrate incoming signals: coordinates emesis)
18
Q
list 5 different triggers of nausea/ vomitting
A
- stimulation of the sensory nerve endings in the stomach and duodenum
- stimulation of the vagal sensory endings in the pharynx
- drugs (Ca chemo, opioids, GA, digoxin)
- disturbances of the vestibular apparatus
- various stimuli of the sensory nn. of the heart and viscera
- others: migraine etc
19
Q
describe the stages of vomiting
A
- nausea - feeling of wanting to vomit, associated with autonomic effects like salvation/pallor/sweating
- retching - strong involuntary effort to vomit with no actual vomiting
- vomiting - expulsion of gastric contents through the mouth
20
Q
what type of vomiting do oesophageal varies and gastric ulcer cause?
A
hematemesis - vomiting fresh blood or altered (ground coffee looking, comes from further down GIT) blood
21
Q
other than hematemesis, name two other types of vomiting. provide examples of underlying causes
A
- projectile vomiting - suggestive of gastric outer or upper GI obstruction
- early-morning - e.g. pregnancy, alcohol dependence, some metabolic conditions (uraemia)
22
Q
what are the 2 factors that need to be considered when prescribing anti-emetics?
A
- cause of the vomiting must be known to prescribe. it is 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
23
Q
a pregnant women with hyperemesis gravidarum required management. what are some of the considerations when using anti0emetics in pregnancy?
A
benefit: risk ratio (mother and foetus)
try and avoid giving in 1st trimester
24
Q
list 4 types of anti-emetic medications based on their mechanism of actions
A
- antimuscarinics (M1)
- antihistamine (H1)
- dopamine antagonists (D2)
- 5HT3 antagonists
25
antimuscarinic anti-emetics:
a) name the location of muscarinic receptors where these drugs will act
b) name an example
c) name a common presentation that the example in b) is usually used for
d) name 4 SEs
a) vestibular nuclei which receives impulses from the labyrinth
b) Hyoscine Hydrobromide (caution in epilepsy)
c) motion sickness (tablets or patches)
d) dry mouth, blurred vision, hot/flushed skin, bradycardia followed by tachycardia, palpitations and arrhythmias
26
antihistamine anti-emetics:
a) when is it useful?
b) list some SEs
c) list 3 examples
a) in numerous causes of N/V; including motion sickness and stomach irritants. if someone has a more generic type, something like this will be prescribed
b) drowsiness, anti-muscarinic effects
c) cinnarixine -->good for vestibular disorders and motion sickness rather than generic N/V, contraindications in porphyria, SEs: drowsiness, nausea, weight gain
cyclizine --> generic N/V, motion sickness, vestibular disorders, palliative care. contraindicated in severe liver disease. SEs = angle closure glaucoma, depression, drowsiness
promethazine --> N+V, motion sickness, labyrinthine disorder, good for severe morning sickness. contraindicated in under 2 y/o. SEs: drowsiness, anxiety, dry mouth
27
dopamine antagonists anti-emetics: list 3 examples
1. phenothiazines e.g. chlorpromazine, prochlorperazine --> any cause, including more severe N/V associated with Ca, radiotherapy drugs. SEs: sedation, hypotension, extrapyramidal symptoms
2. domperidone --> N+V associated with cytotoxic therapy; GI causes. caution if increased GI motility or cardiac disease. SEs: small increased risk of serious cardiac adverse effects, dry mouth
3. metoclopramide --> N/V associated with migraine/ chemo/ radiotherapy and post-op. contraindicated post GI surgery, GI haemorrhage/ obstruction. SEs: movement disorders, fatigue, motor restlessness, spasmodic torticolis, stimulates prolactin release
28
5HT3 antagonists:
a) name the location of receptors where these drugs act
b) name and example
c) name a common presentation the example
d) list SEs
a) prime site of action is the CTZ
b) ondansetron ('ansetron')(contraindicated in congenital long QT syndrome)
c) N/V in pt's receiving cytotoxic, radiation therapy and post op N/V
d) headache, GI upset (uncommon)
29
what are the 2 specific types of gut motility?
1. propulsion (peristalsis)
| 2. mixing (combination of peristalisis and local contractive contractions)
30
describe the implications of chronic constipation
- impedes bowel
- proximal bowel attempt to clear stool via peristalsis waves -> can cause pain and dilation
- overflow may cause Dx of diarrhoea which if treated can have serious consequences
(*before prescribing laxatives, should ensure the problem is constipation, check the pt's 'norm', try to reverse the cause)
31
discuss 4 types of laxatives and give an example
1. Bulk-forming e.g. Ispaghula husk:
- provides increased volume and promotes peristalsis by distension
- indications = small hard stools, fibre cannot be increased in diet
- contraindications = colicky pain, reduced gut motility
- SEs = abdo distension, bronchospasm
2. stimulant laxative e.g. Senna:
- indications: require increased GI motility
- contraindications: abdo cramps, intestinal obstruction
- SEs: diarrhoea, electrolyte imbalance
3. softener laxative e.g. Docusate:
- indications: chronic constipation, allow penetration of intestinal fluid
- contraindications: intestinal obstruction
- SEs: abdo cramps, rash, nausea
4. osmotic laxative e.g. lactulose:
- indications: produce osmotic diarrhoea of low focal pH ( useful in hepatic encephalopathy as ammonia producing bacteria don't like environment)
- contraindications: intestinal obstruction, galactosemic
- SEs: abdo pn, flatulence, N/V
32
acute diarrhoea = abrupt onset of 3 or more loose stools/ day and lasts no longer than 14days.
a) describe the problems associated with acute diarrhoea
b) name possible bacterial causes
a) increased GIT motility
decrease absorption of fluid
loss of electrolytes
b) campylobacter enteritis
shifellosis
samonellosis
Ecoli
33
what is the Tx for ACUTE diarrhoea?
- maintenance of fluid and electrolyte balance (oral rehydration prep)
- anti motility drugs e.g. Loperamide (Imodium). contraindicated in active UC, antibiotic associated colitis, abdomen distension. Yes = GI disorders, headache, nausea
- antispasmodics to reduce muscle tone e.g. Buscopan (hyoscine butyl bromide). contraindicated in tachycardia. SEs skin reactions, dyspnea
34
Chronic diarrhoea is an episode that last >14days.
what is the Tx?
anti motility agens --> loperamide
bulk forming drugs --> ispaghula hull
opioids if associated pain
35
define what its meant by complementary alternative medicine
no universally accepted definition.
NHS -> 'complementary and alternative medicines (CAMs) are treatments that fall outside of mainstream healthcare'
36
outline the range of CAMs therapies
> alternative medical systems e.g. traditional Chinese medicine, homeopathy, naturopathy, indigenous healing systems
> mind-body interventions e.g. yoga, meditation, deep-breathing exercises, tai chi
> biologically based therapies e.g. herbal medications, vegetable juice therapy, bee venom therapy
> manipulative and body-based methods e.g. osteopathy, chiropractic, acupuncture
> energy therapies e.g. healing touch, magnet therapy, light therapy
37
Identify the potential indirect risks associated with complementary alternative medicine
- what is established and evidence based can be difficult
- some CAM modalities can be obtained without practice of practitioner e.g. acupuncture (could be perceived as health professional, and gives healthcare advise)
- medical pleuralism: adoption of more than one medical system to the use of both conventional and complementary and alternative medications (e.g. complexity of interactions with migrants that trust systems back home, which may use forms of CAM, and difficult it it goes against evidence-based advice and interacts with medications provided by the NHS)
38
Discuss the reasons why, and how, patients may use Complementary Alternative Medicines.
reasons:
- chronic long term conditions
- enhancing general sense of well being and overall wellness
- belief that it will be more effective than conventional Tx
- exhausted conventional options or there is no options
- conventional options associated with SEs/ risk (see CT as less natural and herbal is natural and therefore safe)
- feeling of more control
- bridge the gap between illness/disease and waiting time for appointment
- part of health system belief in home country
- longer time with practitioner compared to NHS
39
Identify the potential risks, direct and indirect, associated with specific complementary alternative medicine
1. Homeopathy:
D - no risk of interactions with 'high potency' medications
ID - delay in receiving appropriate Tx
- homeopathic practitioners are more likely to have anti-vaccine views and give advice on this
- no legal regulations to set up clinic. media however, have to be made as described
2. Herbal medicine:
D- interaction with other drugs e.g. contraceptives, anti-depressives, anti-coagulants, anti-epilepsy agents etc
- adverse drug reactions (herbal practitioner can make mix to suit pt's needs - no regulation)
- quality control (potency difference between batches)
ID - delay in receiving appropriate Tx
*regulated
```
3. chiropractic and osteopathy:
D - adverse reaction (50%)
- tearing of artery wall leading to stroke
- injury to spinal cord
- chiropractic X-rays
ID - delay in receiving TX
- practitioner attitudes
* statutory regulation
```
```
4. acupuncture:
D - infections
- pneumathorax
ID - delay in receiving Tx
- attitudes of practitioners
**local authority licensing
```
40
what are the ethical issues surrounding CAM?
does it work?
- nothing more than a placebo, is that a bad thing?
- do we need to know how a treatment works?
is it safe?
- regulation of practitioners/ substances
- direct vs indirect harm
how to balance pt choice against the first duty of a doctor: make the care of your pt's your first concern
- pt autonomy
- informed choice
41
what is the disadvantage of the anatomical positioning of the spleen?
adjacent to ribs 9,10 and 11 on the left side. rib fracture may rupture the spleen, causing considerable intraperitoneal haemorrhage
42
what is the function of the spleen?
1. mechanical filtration of RBCs
2. active immune response through humeral and cell mediated pathways
3. haematopoiesis until 5th month of gestation
4. lymphocyte proliferation
43
why is surgical access to the pancreas difficult?
it lies in the C-shaped curve of the duodenum, extending across the epigastrium very close to major blood vessels
44
where is the surface marking of the gall bladder?
tip of the 9th right costal cartilage
45
what is a potential cause of painless, continuous jaundice
carcinoma of the head of the pancreas - may obstruct the bile duct
46
what embryonic layer is the liver formed from
endoderm (all GI organs)
47
what signs suggest portal hypertension?
oesophageal varcies
haemorrhoids
caput medusae
(portosystemic anastomotic vv. become tortuous and dilated - varicose, and may rupture, leading to catastrophic haemorrhage)
48
what is the natural indentation on Ba swallow between the pharynx and the oesophagus on lateral view
normal function of the cricopharyngeal sphincter - to prevent air being sucked into the stomach during inhalation
49
what 3 structures cause indentations to the oesophagus on BA, oblique view
1. arch of aorta
2. left main bronchus
3. left atrium of heart
50
what a. supplies the lower oesophagus?
left gastric artery, therefore drains into the portal vein making it a site of port-systemic anastomosis
51
what is Hirchsprung disease?
lack of normal development of the colonic innervation leads to constrictied, ganglionic segment of bowel, with a distended segment proximally (innervation of which, is normal)
52
provide another 2 examples of abdominal birth defects
1. Omphalocele:
- failure of the physiological hernia to return to the abdomen; intestine lies outside the abdomen, but in the umbilical cord and covered by amnion
2. Gastroschisis:
- failure of abdominal wall closure following lateral folding; intestine lies completely uncovered, outside the abdomen
53
what is the prevalence of PTSD?
PTSD is an anxiety disorder associated with experiencing or witnessing single, repeated or multiple events (intense and frightening emotional experiences) leads to lasting changes in behaviour, mood and cognition (thoughts, beliefs and attitudes)
- estimated lifetime prevalence of 6.%
- most common traumas are combat fro men and sexual molestation for women
- 25-30% of people who experienced a traumatic event develop PTSD
54
what are the main clinical features of PTSD?
NICE: be aware that people with PTSD, and complex PTSD (related to a series of events compared to a single event), may present with a range of symptoms associated with functional impairment, including:
- re-experiencing, avoidance, hyperarousal, emotional numbing dissociation, emotional dysregulation, interpersonal difficulties or problems in relationships, negative self perception
- feelings of guilt, shame, sadness, betrayal, humiliation and anger
55
discuss some of the main management strategies of PTSD
trauma-focussed psychological Tx (1st line):
-> trauma focused CBT - up to 12 sessions. combination of exposure therapy (confront traumatic memories and repeatedly exposed to situations which they have been avoiding that elicit fear) and trauma-focussed cognitive therapy (identifies and modifies misrepresentations of the trauma and its aftermath that lead the person to overestimate the threat)
eye movement desensitisation and reprocessing:
-> up to 12 sessions. uses bilateral stimulation (eye movements, taps and tones) while the person focuses on memories and associations. this is thought to help the brain process flashbacks and to make sense of the traumatic experience.
56
define the term 'resilience'
adult capacity to maintain healthy psychological and physical functioning
- majority of adults are exposed to at least one potentially traumatic event in their lifetime. most experience confusion and distress, only a small subset of exposed adults develop ptsd
57
what are the risk factors of PTSD?
- exposure to a traumatic event
- severity of the incident
- female
- young age
- previous experience of trauma
- presence of multiple major life stressors
- low social support
- Hx of mental health
58
give 3 examples of some of the main categories of psychiatric disorders
1. mood disorders - fundamental disturbance in a change in affect or mood to depression ( ± associated anxiety) or to elation. often associated with change in level of activity
2. behavioural syndromes - anorexia nervosa, bulimia nervosa, overeating associated with other psychological disturbance
3. organic disorders - decreased mental function due to medical or physical disease of the brain, rather than psychiatric illness e.g. delirium, dementia and amnesia
59
describe some of the advantages and disadvantages for classifying mental disorders
advantages:
- standardises diagnos and treatment (ensure pt;s receive appropriate helpful treatment regardless of location or social class)
- guides research
- guides therapy
- strict criteria increases reliability (I'm statistical content)
- improve agreement between assessors
disadvantages:
- oversimplifies human behaviour (lose track of unique human element)
- risk of misdiagnosis or over diagnosis because sometimes behaviours don't line up with current ideal
- labels can be stigmatising
60
what is meant by zone of rarity
chasm that separates various diagnostic categories from each other and from normality is called the “zone of rarity.” Using this concept there should be a clear demarcation between those who are ill and those who are not, with few, if any, individuals in the intermediate zone.
(no zone of rarity in depression because there is no biomarker)
61
define weight loss
loss of 5% body weight overt 6months
62
catagorise the causes of weight loss and give an example for each
Psychosocial:
- eating disorders
- bereavement
- depression
- substance misuse
- neglect
gastrointestinal:
- oral problems
- malabsorption
- malignancy
- inflammatory bowel disease
- liver disease
endocrine:
- diabetes
- hyperthyroidism
- addison's disease
cardiac/rep/renal/neurological:
- COPD
- Heart failure
- advanced ckd
- neurodegenerative disease
systemic inflammation:
- vasculitis
- SLE
- RA
- temporal arteritis
infection:
- TB
- GI infections/ infestations
- HIV/AIDS
malignancy:
- colorectal
- gastro-oesophageal
- prostate
- pancreatic
- lung
- urological
medication:
- metformin, SSRIs, anti-cancer
- drugs of misuse
- alcohol
- herbal medicines
63
what would be included in a focused Hx from a pt presenting with weight loss
how much weight loss?
how long?
pattern?
intended?
ask specifically about previous ca, hyperthyroidism?
medications?
systems review important - decreased appetite/early satiety, oral problems; dysphagia, dyspepsia, abdominal pn, change in bowel habits; constipation, diarrhoea, bloating, PR bleeding; fresh or mixed with stool, altered blood. cough, haemoptysis, SOB, oedema, chest pn. lower urinary tract symptoms, visible haematuris, loin pn, vaginal bleeding. fever, night sweats, tiredness/lethargy
64
what would be included in a focussed physical exam in a person presenting with weight loss
```
document weight
old records might be helpful
clubbing (malignancy - broncho carcinoma. infections - emphysema, bronchiectasis. IBD)
nail infarcts (systemic vasculitis)
temperature (warm vasodilator hands typical for hyperthyroidism)
pulse (tachy; thyrotoxic cause)
stigmata of liver disease
pallor
jaundice
eye signs
dentition, ulcers, thrush
cervical nodes (left supraclavicular node is enlarged in intra-abdominal malignancies, breast ca and infection)
breast exam
skin changes/rash?
abdo exam
resp/CV exam
```
65
discuss when and how to Ix weight loss
no single Ix
pick up clues from Hx and exam
simple start = urinalysis
glucose - diabetes
proteinuria - renal disease
haematuria - intrinsic renal disease, urological malignancy
pence-jones protein - myeloma
FBC - anaemia ( microcytic iron def or potential chronic blood loss that cold lead to that)
MCV - macrocytosis can be sign of vita def (B12) or alcoholism
WBC - raised in infection and inflammatory conditions
eosinophil - vasculitic process or parasite/helmith infection
platlets - low in liver disease. increase in chronic and systemic inflammatory conditions
LFTs
U+E's
TFT
CPR/ESR
Calcium - hypercalcaemia is a feature of malignancies esp myeloma
```
CXR
FIT
PSA/CA125
CT
endoscopy
```
66
CASE 1
64 y/o man present complaining of significant w.loss over 6mnths. he also complains of fatigue. on questioning, he tells you that he has had occasional fever, night sweats and hemoptysis. long standing LUTS.
O/E: thin, pallor, no palpable lymphadenopathy. no jaundice or clubbing. CVS/RS/GIS normal.
what are the DDx? and what Ix would you request?
DD - lung Ca, TB, lymphoma (night sweats and fever)
LUTS may not be linked in this case
CXR would be appropriate
67
CASE 2
A 38 year old woman who presents to her GP with weight loss over the last 3 months (about 7kg). Her usual weight is around 63kg, confirmed by looking at old records.
She also reports being tearful and anxious a lot. She had attributed these symptoms to feeling sad about the death of her mother a few months earlier, but her symptoms have not improved. She think she is eating well – possibly more than normal - and has not changed her exercise pattern.
You ask her some questions about her health in general. She has no GI/RS/CVS/GUS symptoms. She is on no regular medication and denies any illegal drug use or use of any OTC/CAM treatments.
O/E
Afebrile, Pulse 110 regular, BP 115/70, resting tremor
Diffusely enlarged thyroid gland, no palpable goitre
Bilateral exophthalmos with swelling and erythema of the eyelids
what is the likely Dx?
hyperthyroidism with classic Hx of weight loss despite increased appetitie and eye signs
do standard Ix but expect to see abnormalities in thyroid tests
68
A 28 year old woman presents on several occasions to her GP with non- specific symptoms including fatigue, anorexia, generalised weakness and weight loss. This has been going on for 8 months. She’s anxious that she might have a thyroid problem (as her mother has) and asks that her thyroid function is checked.
Examination findings: BP 105/60, pulse 100, thin. She has hyperpigmentation of her buccal mucosa.
What is the likely Dx?
long hx of non-specific symptoms but progressive weight loss. low BP and hyperpigmentation, this could be Addisons disease
69
A 19 year old student brought in by his mother to the emergency department. She is worried that he has become a bit confused since returning home from college today. She tells you that this is on the background of 2 weeks of lethargy and marked weight loss over at least a month. She has also noticed him drinking a lot of water and juice over the last week and complaining of constant thirst. He has become more unwell over the last hour, with nausea and vomiting. He has no significant past medical history, and is not on any prescribed medication.
Examination findings include the following: BP 90/64, pulse 120, dry tongue. You notice a strange pattern of breathing. His is alert but seems slightly confused at times when you ask him questions.
what is the likely Dx?
che ck glucose. potential new Dx of diabetes classic Pcx of polydipsia, polyuria and weight loss
check ketones on bloods as well
70
A 62 year old man presents with weight loss over several months. He initially began to notice that his trousers were getting loose. His wife had also noticed this weight loss saying that his clothes all looked too big for him and urged him to seek medical advice. He ’didn’t want to make a fuss’ so delayed things for a few weeks and tried to eat a bit better.
Before getting a chance to see his doctor, his wife noticed one morning that had a ’yellow tinge to the whites of his eyes’. He visits his GP later that day. Urgent blood tests show the following:
Bilirubin – 116 μmol/ L ALP – 347 U/L
ALT – 40 U/L
what is the likely Dx?
obstructive picture of jaundice. in context of significant weight loss needs urgent Ix. Ca of head of pancreas until proven otherwise
CT scan for pancreas
(USS for liver)
71
A 52 year old man presents with a 6-month history of unintentional weight loss. He has lost around 5 kg in weight, having previously weighed around 90kg. This has recently stabilised and he has not lost any more weight since he came one month ago for an initial consultation. He is otherwise well, although he is becoming increasingly anxious about the cause of his weight loss. He has been eating more healthily over the last few months but doesn’t think that is enough of a reason to explain his symptoms.
Systems review - unremarkable
Examination – BMI in normal range, CVS/RS/GIS normal
Initial tests:
Normal FBC/creatinine/electrolytes/LFTs/TFTs/CRP/ESR
what is the likely Dx?
More difficult because there are very few pointers in Hx to suggest particular Dx. Reassured that all the initial tests are normal. Reassuring that weight loss has not progressed since he was consulted a month ago. Full discussion with pt on how you would proceed. Might be a case where you monitor things and see where things go.
72
when does normal eating variance become an eating disorder?
not just eating too much or too little. unhealthy focus on eating, their body, their weight and their shape.
73
describe the different types of eating disorders and the clinical features and classification
DSM-5 diagnosis:
1. Avoidant-restrictive food intake disorder (ARFID)
- characterised by lack of interest in food, fear of negative consequences of eating (choke/vomit), and selective eating.
- persistent failure to meet appropriate nutritional requirements and 1 or more of the following;
i) significant weight loss/ failure to gain/ faltering growth
ii) significant nutritional deficiency
iii) dependence on supplements
iv) interference with psychosocial functioning
- not explained by cultural practice/ lack of food
- no disturbance of perception of body weight/shape
- not due to medical condition
2. anorexia nervosa:
characterised primarily by self-starvation excessive weight loss:
- signs: dramatic weight loss, preoccupied with weight, food, calories and diet, refusal to eat certain foods, excuses to avoid mealtimes, inappropriate +/or extreme exercise
- 3 criteria for Dx of AN;
i) restriction of energy intake relative to requirements leading to a significant low body weight in the context of age, sex, developmental trajectory and physical health
ii) intense fear of becoming fat or gaining weight; persistent behaviour interfering with weight gain despite being low weight
iii) disturbance in the way ones body weight or shape is experienced; undue influence of body weight or shape on self-evaluation, or persistent lack of recognition of the seriousness of current low body weight
- subtypes = restricting vs bing-eating/purging
3. Bulimia Nervosa:
- characterised by binge eating and compensatory behaviours, such as self-induced vomiting, in an attempt to undo the effects of binge eating (most are normal weight)
- symptoms: frequent consumption of large amounts of food followed by behaviours to prevent weight gain, such as vomiting, laxative abuse, and excessive exercise. feeling of being out of control when binging. extreme concerns with body weight and shape.
- classification/criteria:
i) recurrent ep's of binge eating: 1. eating more than what most people would eat in similar circumstances in discrete period of time. 2. lack of control over eating during the ep.
ii) recurrent inappropriate compensatory behaviours to prevent weight gain
iii) i and ii occur on average once a week for 3mnths
iv) self evaluation is unduly influenced by body shape and weight
v) the behaviour doe not occur exclusively during eps of AN
4. Binge Eating disorder
- many of the same classification of bulimia but no compensatory mechanisms
- classification/ criteria:
i) recurrent eps of binge eating characterised by: 1. eating more that what most people would eat in similar circumstances in discrete period of time. 2. lack of control over eating during the ep.
ii) binge eating eps associated with 3 or more of: 1. eating more rapidly than normal; 2. eating until uncomfortably full; 3. eating large amounts when not hungry; 4. eating alone due to embarrassment; 5. feeling disgusted, depressed, guilty afterwards
- marked distress over binge eating
- occurs on average once a week for 3months
- no inappropriate compensatory behaviours nor exclusively during the course of BN or AN
74
describe the epidemiology and aetiology of eating disorders
epidemiology:
- 1.25 million people in uk have eating disorder
- girls and young women 12-20 most at risk
aetiology:
- biological factors: gender (F>M), genetics (mono>dizygotic twins), co-morbidities e.g. depression, anxiety, OCD, T1DM
- psychological factors: low self esteem/ poor relationship with self, poor coping mechanisms, personality traits e.g. perfectionism, obsessive thinking, rigidity
- social factors: historical trauma, sexual abuse, trauma, peer pressure, body shaming/weight stigma, media/modern culture
**Early intervention is key
75
describe assessment of disordered eating and how eating disorders are diagnosed
entire psychiatric assessment - focus on eating and the thoughts behind it
essential details:
- what are you worried about? and why?
- current eating and its progression
- current weight (+height) past weights and idea of how quickly being lost
- impact on physical health
- cognition around eating and weight
- any significant stressors
- co-morbidities (physical or mental health)
- do decent physical health assessment including bloods!
* MARSIPAN = tool for assessing how severe disorder is
- incorporated recent weight loss, syncope, fluid and food intake, exercise habits, suicidal ideas, acute co-morbidity, % weight for height , heart rate, blood pressure, ECG, electrolyte disturbance, muscle weakness
76
describe the physical effects of eating disorders of different body systems
CV:
- muscle loss
- low or irregular heartbeat
gastrointestinal:
- gastroparesis = bloating, nausea, feeling full after only small amounts, constipation
neurological:
- brain consumes up to 1/5th of body calories. difficulty concentrating, sleep apnoea
endocrine:
- hormonal changes - oestrogen, testosterone, thyroid
77
what are treatment options for young people and families dealing with eating disorders?
AN:
> provide support and care for all people with AN in contact with specialist services, whether or not they are having a specific intervention. support should:
- include psychoeducation about the disorder
- include monitoring of weight, mental and physical health, and any risk factors
- be multidisciplinary and coordinated between services
- involve the person's family members or carers (if appropriate)
> when treating AN, be aware that:
- helping people to reach a healthy body weight or BMI for their age is a key goal AND weight gain is key in supporting other psychological, physical and quality of life changes that are needed for improvement or recovery
>consider:
- refeeding syndrome risk
- consequence of starvation on developing brain and cognition
- therapy for depression
- family-based therapy (most effective)!
>motivation!
- help children see links between anorexia and symptions
- help children see benefit of weight gain
>medication:
- food (taken in amounts prescribed and at the times specified) oral if possible
>outpatient care if pt is medically stable
BN:
>CBT targeting bulimic symptoms = gold standard
78
what is referring syndrome?
potentially fatal shift in electrolytes and fluids
malnourished pt's are fed too quickly
hypophophatemia, hypomagnesemia, hypokalemia, gastric dilation, congestive cardiac failure, severe oedema, confusion, coma, death
adequate monitoring, especially phosphate
the most at risk are:
- pt's with very low weight for height
- minimal or no nutritional intake for more than a few days(3-4)
- weight loss of over 15% in the last 3 months
- those with abnormal electrolytes prior to re-feeding
signs:
- bradycardia, hypotension, hypophophatemia, delirium, oedema, cardiac arrhythmia
79
define hyponatraemia and the clinical features
normal range of sodium is 134-145mmol/L
```
hyponatraemia = Na <135mmol/L
-> mild = 130-135
-> moderate = 125-129
-> severe = <124
(acute <48hrs, chronic >48hours)
-> most common electrolyte disorder!
-> can be asymptomatic; symptoms correlate with severity and speed of onset I.e. when plasma osmolality falls quickly, water rapidly flows into cerebral cells causing swelling; gradual onset allows cerebral cells to reduce intracellular osmolality
- none --> nausea, confusion, headache --> coma, seizures, vomiting
```
80
list causes and pathophysiology of hyponatraemia
- hypovolaemia - pt is dehydrated/ loss of blood volume; deficient in water and Na. D+G, skin burns, diuretics, NG suction, adrenocorticol failure
- euvolaemia - water increase, but Na stays the same. no oedema. causes = SIADH*, polydipsia, iatrogenic - IV fluids
- hypervolaemia - water and Na increase in the body. fluid vol overload. will see swelling. However, Na becomes diluted (total body water and Na are regulated differently). causes: heart, failure, cirrhosis of liver, CKD
81
what is SIADH?
syndrome of inappropriate ADH secretion
- ADH promotes water retention in the distal tubule
- released in response to increasing plasma osmolality
- SIADH causes excess water retention without a physiological cause resulting in hyponatraemia
- causes: tumour, CNS infection, lung disease, drugs, idiopathic
82
what other causes of non-hypotonic hyponatremia must be excluded?
hyperglycemia
83
what are the management options for hyponatraemia?
- depends on severity, acuity and underlying cause
- acute onset with signs of cerebral oedema - prom correction with hypertonic saline
- if chronic, rapid overcorrection can be very dangerous, so slow correction is key (<10mmol/L/24h)
- correct hypovolaemia (saline hypertonic solution)
- evolaemic/hypervolaemic - fluid restriction
84
define hypernatraemia
Na>145mmp;/L
severe = >160mmol/L
85
describe the aetiology and pathophysiology of hyernatraemia
free water loss
- renal: osmotic diuretic
- GI: diarrhoea
- skin: sweating
- diabetes insipidus
inadequate intake:
- limited access to water
excess NA:
- excessive salt IV or oral
86
how would you IX and Mx hypernatreamnia?
Ix:
- electrolyte, glucose, renal biochem, urine/serum osmolality, urine electrolytes
- desmopressin challenge test (test for diabetes insipidus cause of hypernatraemia)
- MRI or CT brain
Mx:
- depends on the cuase
- oral fluids
- IV fluids with caution
- diuretics if excess Na due to IVF
87
define hyperkalaemia
normal potassium in serum is 3.5-5.5mmol/L
- > mild = 5.5-5.9mmol/L
- > moderate = 6-6.4mmol/L
- > severe = >6.5
- major intracellular cation
- crucial for normal functioning go nerves, muscle and heart
88
what are the clinical features and Ix go hyperkalaemia?
mild - moderate is usually asymptomatic
severe can cause muscle weakness, collapse/arrest/arrythmia
Ix:
- blood tests; creatinine/eGFR, sodium, bucarbonate
- ECG!
89
what is the aetiology and pathophysiology of hyperkalaemia?
excessive intake:
- dietary K+ (but usually only a problem if there is reduced excretion)
- IV fluids
inadequate excretion:
- reduced eGFR -> AKI/CKD,
- reduced aldosterone -> Addison's, ACE-I, ARB, spironolactone
- renin inhibition - NSAIDs/BB
redistribution:
- acidosis
- insulin deficiency
- rhabdomyolysis
- tumour lysis syndrome
90
what is the management of hyperkalaemia?
stabilise the cardiac membrane with IV calcium glauconite
shift K into cells with salbutamol, IV insulin/dextrose, bicarbonate
remove K from body with fluid resuscitation, ion-exchange resin (PR/PO), dialysis
91
define hypokalaemia and its clinical features
<3.5mmol/L
3-3.4mmol/L is asymptomatic
severe - muscle weakness and tiredness, paralytic ileus
92
what is the aetiology of hypokalaemia
excess loss urine:
- mineralocorticoid excess - Conns syndrome
- genetic cause
- diuretics - loop/thiazide
excess loss GI:
- upper - vomiting, NG aspiration
- lower - diarrhoea, laxative abuse
inadequate intake:
- dietary deficiency e.g. AN
- IV fluids
redistribution/ internal balance shift:
- alkalosis (metabolic)
- insulin
- beta agonist (salbutamoll)
93
Ix of hypokalaemia
blood tests:
- bicarbonate, mg, Ca
- ? renin
- urinary K
ECG
94
define hypercalcaemia and its clinical features
>2.6mmol/L
normal = 2.1-2.6mmol/L
bound to albumin, so level needs to be corrected for hypoalbuminaemia
CF:
- > Bones, Moans Groans and Stones...
- musculoskeletal pain
- depression
- abdominal pain
- renal colic
- can present acutely with severe hypercalcaemia and dehydration
95
what are the causes of hypercalcaemia?
Normal or high PTH:
- primary hyperparathyroidism (single adenoma)
- tertiary hyperparathyroidism
low PTH:
- malignancy - lung, breast, renal, lymphoma, myeloma
- thyrotoxicosis
- thiazide diuretics
- sarcoidosis
96
what are the Ix and Mx of hypercalcaemia?
- PTH is key
- renal function (teritiary hyperparathyroidism)
- screen for malignancy - CXE, myeloma screen, CT
Mx:
- treat underlying cause
- urgent management
97
what are the clinical features of hypocalcaemia?
- mild is usually asymptomatic
- severe -> muscle spasm and tetany
signs = Trousseau's sign ( carpopedal spasm caused by inflating the blood-pressure cuff to a level above systolic pressure) and Chvostek's sign (twitching of the facial muscles after tapping of area over facial n.)
98
what are some of the causes of hypocalcaemia?
chronic renal failure - impaired vic D hydroxylation, tased PTH
hypoparathyroidism - most commonly iatrogenic
pseudohypoparathyroidism - tissue resistance to PTH
hypomagnesaemia - affects ability of PT glands to secrete PTH
Mx:
- depends on cause. e.g. treatment of renal bone disease
- emergency Mx of severe hypocalcaemia - IV calcium gluconate
99
discuss hypo and hypermagnesaemia
HYPO
- <0.75mmol/L
- mild is asymptomatic, severe -> tetany
- inadequate intake: malnutrition, excessive loss: urinary/GI, other: PPI, pancreatitis
- Ix = ECG
- Mx = IV Mg
HYPER
- >1mmol/L
- bradycardia, hypotension
- causes = Mg containing medications
- Mx = promote renal excretion
100
discuss hypo and hyperphosphataemia
HYPO:
- <0.8mmol/L
- wide-ranging CFs
- redistribution to cells -> reseeding syndrome; inadequate intake -> malnutrition, phosphate binders; increase excretion -> primary hyperparathyroidism
- Mx = oral su[plementation, IV in critical care
HYPER:
- >1.4mmol/L
- CF = pruritus, long term calcium phosphate deposition
- AKI or CKD
- Mx = dietary restriction, phosphate binding drugs
week 37: weight loss
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