1
Q
measuring w t1?
A
- measure HbA1c levels every 3 to 6 months in adults w T1DM
- target of 48mmol or lower
- offer a cont monitoring or a intermittently scanned cont glucose mnonitoring
2
Q
self monitoring w t1?
A
- at least 4x a day
- before each meal and before bed
3
Q
glucose aims w t1?
A
- a fasting plasma glucose level of 5 to 7mmol/litre on wakingand
- a plasma glucose level of 4 to 7mmol/litre before meals at other times of the day.
4
Q
DKA initial management?
A
- isotonic saline for primary fluid replecemenr therapy - not given too rapidly except in cases of circulatory collapse
- iV insulin infusion
- potassium replacement therapy
5
Q
first line in diabetics w HTN ?
A
ACEi - renoprotective effects
6
Q
insulin regime of choice for t1?
A
- Offer multiple daily injection basal–bolus insulin regimens as the insulin injection regimen of choice for all adults with type1 diabetes
- Offer twice‑daily insulin detemir as basal insulin therapy for adults with type1 diabetes
7
Q
primary care in diabetes Mx?
A
- services include regular monitoring, diabetic education, lifestyle advice, and medication management
- GPs, practice nurses, dietitians
8
Q
secondary care in diabetes?
A
- more specialised
- diabetic clinics, endocrinology departments, MDTs - endocrinologists, diabetic specialist nurses, dietitians, podiatrists, and opthalmologists
- Secondary care offers more complex management, including insulin pump therapy, continuous glucose monitoring, and management of diabetic complications.
9
Q
variation in diabetes services?
A
- urban areas have better accesse to specialised diabetes clinics
- higher levels of deprivation may exp higher level of diabetes - more deprived areas may have fewer resources for diabetes prevention and manageemnt
- variation in primary care capacity
10
Q
what varies between regions?
A
- The presence of community-based diabetes support groups, educational programs, and lifestyle intervention services can vary between regions, impacting the level of support available to individuals living with diabetes and their families.
11
Q
models of diabetes care - ICP?
A
- ICPs: collaboration between primary and secondary care providers to ensure seamless and co-ordinated care for individuals with diabetes
12
Q
models of diabetes care - MDT approach?
A
- MDT approach: aim to address the complex needs of individuals with diabetes through a holistic and collaborative approach.
13
Q
models of care - primary care led model?
A
- Primary care led model: involve regular monitoring, lifestyle advice, medication management, and coordination of referrals to specialist services as needed.
14
Q
models of care - specialist diabetes centers?
A
- specialist diabetes centers: including advanced treatments, education programs, and support services.
- Specialist diabetes centers may provide outpatient clinics, inpatient care, and access to cutting-edge technologies for diabetes management.
15
Q
UKPDS?
A
- the UK Prospective Diabetes Study (UKPDS) have shown that tight BP control significantly reduces the risk of cardiovascular events, such as heart attacks, strokes, and heart failure.
- renal function - trials have shown that medications targeting the renin-angiotensin system (e.g., ACE inhibitors, ARBs) can delay the progression of diabetic kidney disease.
16
Q
DCCT trial?
A
- reduction in microvascular complications: DCCT trial showed delayed onset and slowed progression of these complications
- CV risk reduction - While the evidence for cardiovascular risk reduction with glycemic control is less consistent compared to blood pressure control, some studies suggest that tight glycemic control may reduce the risk of cardiovascular events over the long term
17
Q
DCCT - improved QOL?
A
- improved QOL - Better glycemic control is associated with improved quality of life, reduced symptoms of hyperglycemia (e.g., polyuria, polydipsia, fatigue), and decreased risk of acute complications,
18
Q
Symptoms of T1D?
A
- Polyuria & polydipsia
- Weight loss
- Vomiting
- Lethargy
19
Q
signs of T1D?
A
- Mild-moderate dehydration (dry skin, dry mucous membranes, reduced skin turgor)
- BMI < 25
20
Q
DKA symptoms?
A
- Confusion
- Moderate-severe dehydration (sunken eyes, prolonged capillary refill time)
- Vomiting +/- diarrhoea
- Abdominal pain
- Decreased urine output
- Reduced GCS
- Coma
21
Q
signs of DKA?
A
- Shock(tachycardia, hypotension)
- Kussmaul breathing(Deep sighing respiration)
22
Q
autoab in T1D?
A
- Islet cell antibodies(ICA)
- Glutamic acid decarboxylase(GAD) antibodies - most common
- Insulin antibodies(IAA)
- IA-2 antibodies(target protein tyrosine phosphatase)
23
Q
Which ppts should be investigated for pancreatic cancer?
A
Patients ≥60 years old presenting with weight loss and new-onset diabetes should be investigated for pancreatic cancer (e.g. CT/MRI imaging of the pancreas).
24
Q
insulin regimes - basal-bolus?
A
- Basal-bolus regime:typically involves the use of rapid- or short-acting insulin before meals and a long-acting preparation for basal requirements.
- This regime is thought to best mimic the physiological function of the pancreas in response to meals and provides better flexibility in control of blood glucose
- It is the standard approach for patients newly diagnosed with T1DM.
25
biphasic regime of insulin?
* One, two, or three injections per day regime: traditionally a biphasic regime with the use of both short-acting and intermediate-acting insulin as separate injections or a mixed product.
26
cont insulin infusion?
* Continuous insulin infusion via a pump: supplies rapid- or short-acting insulin.
* It may be used in patients who are experiencing troubling hypoglycaemic episodes with multiple daily injections regimes.
27
monitoring for complications of diabetes?
* Retinopathy: annual screening
* Nephropathy: renal function (eGFR) and albumin:creatinine ratio (ACR)
* Diabetic foot problems: full examination including footwear, monofilament assessment of neuropathy, vascular assessment +/- dopplers.
* Cardiovascular risk factors: primary/secondary prevention strategy with optimisation of blood pressure, lipids, weight, smoking and others
* Thyroid disease: screening blood test
* Dental disease (periodonitis): advise regular oral health review
28
diabetic foot?
* Diabetic foot complications arise from a combination of neuropathy, PAD, and impaired wound healing.
* They can result in foot ulcers, infections, and ultimately, amputations.
29
management of diabetic foot?
* Proper foot care, early detection and treatment of ulcers, and multidisciplinary care are crucial to preventing severe outcomes.
30
diabetic nephropathy?
* diabetic nephropathy
* characterized by albuminuria, declining glomerular filtration rate (GFR), and eventually, renal failure
31
Management of diabetic nephropathy?
ACE or ARB used
32
insulin adjuncts - when should metformin ve added in T1D?
* they have a BMI of 25 kg/m2 or above (23 kg/m2 or above for people from South Asian and related family backgrounds) and
* they want to improve their blood glucose control while minimising their effective insulin dose.
33
What is obesity?
* disease when excessive body fat results in pathogenic structural or functional abn resulting in increased ppt morbitiy and mortality
34
advantages of using BMI?
* inc BMI generally correlates w metabolic and fat mass diseases in population studies
* commonly used
* reasonably reprod and low cost
* adequate screenign metric for most patients
35
Disadvantages of using BMI?
* may not correlate w metabolic and fat mass diseases in an indiv ppt
* does not account for muscle mass
* cut off points don't distinguish between men and women, nor ethnic and racial considerations
* shouldn't be used as a sole measure of obesity
36
obesity - history:
image
37
physical exam for obesity
vital signs
* Waist circumference
* neck circumference
* height and weight
* BP
* pulse
38
nutritional therapy for obesity?
* very low calorie diets
* reduces glucose, insulin
* reduces bp
39
risks of obesity?
* cold intolerance, dysmenorrhea
* faigue, hair loss, brittle nails
* small inc in gallstones, kidney stones and gout flare
40
exercise prescription (FITTE)
* frequency
* intensity
* time spent
* type
* enjoyment level
41
Meds for obesity?
* Orlistat: lipase inhibitor
* liraglutide: GLP-1 analogue
42
# indications
Bariatric surgery for obesity?
* BMI of >35 with >1 AHC
* BMI of > 40 w or without AHC
43
dietary recommendations for obesity?
* calorie deficit
* portion control
* balanced diet
* limiting energy dense foods - reduce consumption of sugary snacks, fried foors, processed meats, sugary beverages
* inc fiber intake - fruits, veggies, nuts
* limit sugar and saturated fats
* regular meal timings w balanced snacks throughtout the day
* health deating patterns - meditteaenan diet or dietary approaches to stop HTN (DASH)
44
Weight gain occurs when there's an imbalance in?
* energy imbalance - Weight gain occurs when energy intake (calories consumed) exceeds energy expenditure (calories burned
* high calorie food and sedentary lifestyle
45
weight gain - environment?
* obesogenic environment - environment is characterized by an abundance of energy-dense, processed foods high in sugar, fat, and salt, as well as easy access to fast food outlets, vending machines, and convenience stores.
46
SE factors in weight gain?
* SE factors - individuals from lower-income households facing greater barriers to accessing healthy foods, safe recreational spaces, and healthcare service
47
food deserts and weight gain?
* Limited resources, food insecurity, and neighborhood environments characterized by food deserts and limited opportunities for physical activity contribute to higher obesity rates in socioeconomically disadvantaged populations.
48
psychological factors in weight gain?
* psychological factors - stress, depression, anxiety, and emotional eating, can influence eating behaviors and contribute to weight gain.
49
coping mechanisms & weight gain?
* Unhealthy coping mechanisms, such as using food as a reward or comfort, and maladaptive dietary patterns, such as binge eating or night eatin
50
cultural and social norms in weight gain?
* cultural and social norms - Cultural celebrations, social gatherings, and food-centric traditions may promote overeating and contribute to weight gain in Western societies.
51
Why is prev of obesity inc in western society?
* changes in diet - shift towards energy dense, saturated fats and processed carbs
* sedentary lifestyles - desk jobs, screen time, and motorized transportation
* obesogenic envir - fast foods, vending machines, convenience stores
* marketing and advertising of unhealthy foods paticularly to children and adolescents
52
Social implications of obesity?
* stigma -> negative pscyhological effects
* economic burden on society - healthcare costs, reduced productivity
* barriers to accessing opportunities like employment
* healthcare system strain
* productivity loss - absenteeism, disability related limitations
* educational attainment - bulling, exclusion
53
social impacts of obesity - healthcare disparities?
* healthcare disparities - Socioeconomic factors can influence access to healthcare services and resources for managing obesity, leading to disparities in treatment and outcomes among different socioeconomic groups.
54
physical implications of obesity?
* chronic disease risk
* osteoarthiris
* metabolic syndrome
* resp issues e.g. Obst sleep apnoea
* GORD
* depression, anxiety, body image issues, social stigma, and reduced quality of life.
55
economic impacts of obesity - healthcate?
* healthcare costs - increased utilization of medical services, including hospitalizations, doctor visits, medications, and treatments for obesity-related conditions such as diabetes, heart disease, and joint problems
56
economic impacts of obesity?
* Productivity loss
* disability payments
- economic disparities
57
economic disparities and obesity?
* economic disparities - Obesity disproportionately affects socioeconomically disadvantaged populations, exacerbating existing inequalities in access to healthcare, education, employment opportunities, and healthy food options
58
what are the population impacts of obesity?
* public health burden
* reduced life expectancy
* socioeconomic disparities
* interconnected health risks
* childhood obesity epidemic
59
Strategies for reducing obesity - info?
* Providing information and resources on nutrition, physical activity, and weight management through workshops, seminars, educational materials, and online platforms to raise awareness and empower individuals to make healthier choices.
60
strategies for reducing obesity - envir change?
* environmental change - Implementing environmental modifications to promote physical activity and access to healthy foods, such as building walking paths and bike lanes, creating community gardens, improving access to fresh produce through farmers' markets or corner stores, and limiting the availability of unhealthy foods and sugary beverages in schools and public spaces.
61
strategies for reducing obesity - partnerships?
* Building partnerships and collaborations with local stakeholders, including healthcare providers, schools, employers, faith-based organizations, and community leaders, to leverage resources, share best practices, and mobilize support for obesity prevention efforts.
62
Behavioural interventions of obesity?
* self-monitoring of behaviour and progress
* stimulus control
* goal setting
* slowing rate of eating
* ensuring social support
* problem solving
* assertiveness
* cognitive restructuring (modifying thoughts)
* reinforcement of changes
* relapse prevention
* strategies for dealing w weight gain
63
Physical activity in order to manage obesity?
* to avoid obesity people may need to do 45 to 60 minutes of moderate-intensity activity a day, particularly if they do not reduce their energy intake.
* Advise people who have been living with obesity and have lost weight that they may need to do 60 to 90 minutes of activity a day to avoid regaining weight
64
# use when
Liraglutide?
* BMI of at least 35
* or BMI of at least 32.5 in certain ethnic groups and non diabetic hyperglycaemia (42-47) and high risk of CVD
* once daily subcutaneous injection
65
side effects of liraglutide?
* gallstone disorders
* vomiting
* acute pancreatitis
* diarrhoea
66
# used when
orlistat?
* BMI of 30+
* or 28+ with more RF
67
side effects of orlistat?
* abd pain - may be minimised by reduced fat intake
* anx
* diarrhoea
* GI disorders
68
# used when?
semaglutide?
* at least 35
* Lower BMI thresholds for people from South Asian, Chinese, other Asian, Middle Eastern, Black African or African-Caribbean family backgrounds
69
side effects of semaglutide?
* cholelithiasis
* GI disorders
* hypoglycaemia
* weight decreased & appetite dec
70
# Indications
surgical interventions for obesity?
* BMI over 40
* Or between 35-40 with a sig health condition
* lower BMI threshold for South Asian, Chinese, other Asian, Middle Eastern, Black African or African-Caribbean ppl
71
types of bariatic surgery?
- laparoscopic adjustable gastric banding
- sleeve gastrectomy
- Roux-en gastric bypass
- billiopancreatic diversion
72
Laparoscopic adjustable gastric banding (LAGB)?
* Band is placed around the stomach at the proximal end, creating a small pouch at the top of the stomach.
* Band can be adjusted over time to alter the amount of restriction
* Adjustments made by injecting or withdrawing fluid from a subcutaneous access port
73
What is the safest and least invasive type of bariatic surgery?
LABG
74
LABG - weight loss peaks at?
18 months post-procedure
75
LABG -
* Can make some foods difficult to tolerate
76
LABG - band related complications?
Slippage, erosion, or leakage of the gastric band, which may require surgical revision or removal.
77
LABG - band intolerance?
Some individuals may experience discomfort, pain, or intolerance to the gastric band, leading to inadequate weight loss or complications.
78
sleeve gastrectomy?
* Part of the fundus and body of the stomach are removed – about 75% of the stomach in total
* Stomach volume typically reduced from 2500ml to 200ml
* Permanent fixed reduction
79
what is required after a sleeve gastrectomy?
* Patients require mulitvitamin, and sometimes iron and B12 supplementation for life
80
risks of sleeve gastrectomies?
- acid reflux
- strictures
81
Acid reflux after a sleeve gastrectomy?
* Acid reflux: Increased risk of gastroesophageal reflux disease (GERD) due to changes in stomach anatomy and increased pressure on the lower esophageal sphincter.
82
Strictures after a sleeve gastrecomy?
* Strictures: Narrowing of the stomach opening or sleeve, which can cause difficulty swallowing and may require further treatment or intervention.
83
Roux-en-Y gastric bypass?
* Small stomach pouch created, and the lower stomach, duodenum and first portion of the jejunum are bypassed.
* Smaller stomach restricts intake
* Bypass of first portion of small intestine reduces absorption of nutrients (and therefore calories intake
84
considerations of RYGB?
* Multivitamin supplementation required for life
* dumping syndrome
* nutrional deficiencies - vitamin B12, iron, calcium, folate
85
biliopancreatic diversion?
* Similar to a Roux-en-Y bypass
* Lower portion of stomach removed and duodenum and first part of jejunum are bypassed
* malabs of ADEK vitamins
86
side effect of bilipancreatic diversion?
* Foul-smelling stools and flatulence: Changes in digestion and absorption patterns can lead to unpleasant digestive symptoms.
87
Dumping syndrome?
Dumping syndrome describes a group of symptoms caused by food rapidly emptying or being ‘dumped’ from the stomach into the small intestines. This results in undigested food within the small intestine that the body finds difficult to absorb.
88
symptoms of dumping syndrome?
sweating, bloating, abdominal cramps/pain, diarrhoea, and nausea.
89
Relationship between impaired glucose tolerance and obesity?
* excess body fat, especially abdmonal can lead to insulin resistance -> hyperglaemia -> development of impaired glucose tolerance -> T2DM
90
Diabetes prevention programme trial found that?
* It demonstrated that lifestyle interventions, such as dietary changes, increased physical activity, and modest weight loss, were more effective than medication in reducing the risk of developing type 2 diabetes among high-risk individuals with impaired glucose tolerance.
* highlighted the crucial role of lifestyle modifications in preventing or delaying the onset of type 2 diabetes
91
NHS diabetes prevention programme?
* recruits patients at high risk of T2DM and refers them to a behaviour change programme
* aims:
* reduce incidence of T2D
* reduce incidence of complications assoc w T2
* to reduce inequalities assoc w incidence of diabetes over the long term
92
Anatomy of the thyroid?
* Comprises 2 lobes connected by an isthmus
* Usually palpable and moves with swallowing
93
physiology of thyroid hormones?
* T4 is converted to T3 in peripheral tissues
* Majority of plasma hormone is bound to transport proteins and is biologically inactive
* Only free hormone is bioactive
94
Hyperthyroidism?
*Excess thyroid hormone production by the thyroid gland
95
thyrotoxicosis=
clinical and biochemical state of thyroid hormone excess – the most common cause of this is hyperthyroidism but it may also be caused by thyroiditis or excess consumption of thyroid hormone tablets
96
causes of hyperthyroidism?
o Grave’s disease
o Multinodular goitre
o Single functioning nodule
o Thyroiditis, including post partum thyroiditis
o Drugs
97
2 main causes of hyperthyroidism?
graves disease and nodular thyroid disease
98
Graves disease epidemiology?
* younger age
* 10x more prev in females
* often familial
99
causes of graves disease?
* Autoimmune disorder (positive thyroid antibodies - TPO and TSH receptor Ab)
* May be self limiting
* Thyrotoxicosis may be severe
100
nodular thyroid disease affects?
* older age
* equal gender ratio
* Rarely familial
* No autoantibodies
101
nodular thyroid disease - onset?
* Gradual onset
* Persistent
* Usually mild
102
symptoms of hyperthyroidism?
* anxiety
* emotional lability
* weakness
* tremor
* palpitations
* heat intolerance, excessive sweating
* diarrhoea
* increased perspiration
* weight loss despite a normal or increased appetite
103
signs of hyperthyroidism in females?
* female: amenorrhoea or oligomenorrhea
104
Eye signs in hyperthyroidism
105
exophthalmos
IMAGE
106
clinical signs in thyrotoxicosis - speech?
* Rapid speech, agitation
107
clinical signs of thyrotoxicosis - eyes?
* Eyes – lid retraction and lag (sympathetic overactivity),
- orbital inflamation (Graves disease)
108
Skin signs of graves?
* Skin – warm and moist, pre-tibial myxoedema (Graves disease)
109
pre-tibial myxoedema?
skin condition that causes plaques of thick, scaly skin and swelling of your lower legs
110
pulse in HT?
* Pulse – tachycardia or atrial fibrillation
111
NM signs of thyrotoxicosis?
* Neuromuscular – tremor, proximal muscle weakness
112
neck signs of hyperthyroidism?
* Neck – presence and size of goitre depends on cause
113
how may old ppl w hyperthyroidism present?
* Older people may present with only weight loss or symptoms of heart failure
114
lab results for hyperthyroidism?
* raised thyroid hormones - usually T3 and T4 but may be only one or the other
* TSH usually suppressed below detection limit
115
ab in hyperthyroidism?
* Thyroid peroxidase antibodies and TSH receptor antibodies
116
thyroid eye disease
* 20% chance of thyroid eye disease
* pain - aching behind the eyeball, aching worse when moving the eye
* redness of the eyelids and of whites of the eye
* swelling in upper eyelids or below eyes
* bulging eyes
* blurred vision
* double visison
117
Medical Tx of hyperthyroidism?
1) carbimazole
2) propylthiouracil - first trimester
118
surgical therapy for hyperthyrodisim?
partial or total thyroidectomy
119
what is given for symptomatic relief for hyperthyrodism?
BB - propanol
120
radiotherapy in hyperthyroidism?
radioactive iodine
121
hypothyroidism?
* most in common females
* Most common form is primary hypothyroidism, but can also be secondary hypothyroidism (hypothalamopituitary failure)
122
lab tests in hypothyroidism?
*Raised TSH
*Reduced FT4 and FT3
*Thyroid peroxidase antibodies (TPO) usually positive in autoimmune disease
123
causes of hypothyroidism?
***** Autoimmune (Hashimoto’s thyroiditis)
* Iatrogenic (surgery, radioiodine treatment)****
* Drugs e.g.
* Directly causing hypothyroidism
* Affecting hormone metabolism
* Affecting gastrointestinal absorption
124
Symptoms of hypothyroidism - slowing of metabolic processes?
cold intolerance, fatigue, weight gain etc
125
hypothyroidism symptoms - tissue deposition?
* tissue deposition of matrix glycosaminoglycans – skin changes, hoarse voice, tongue enlargement etc
126
Extremes of thyroid dysfunction?
* Myxoedema coma – extreme hypothyroidism
* Thyroid storm – extreme thyrotoxicosis
* Both have high mortality
127
Tx of hypothyroidism?
* levothyroxine
* lifelong
128
goitre =
*A goitre is a palpable swelling of the thyroid
*Thyroid lobes grow outward and even very large goitres rarely cause compressive symptoms
*Asymmetric lobe enlargement or a substernal goitre may cause compressive problems
129
Ix for a goitre?
o Fine needle aspiration
o Ultrasound
o Radionucleotide imaging
o Computed tomography/MRI
130
Most common symptoms of a substernal goitre?
- wheeze
- dyspnoea
- cough
131
thyroid nodules are usually noticed when?
* Usually come to light when the person notices a neck swelling or incidentally when detected during a radiological examination of the neck performed for another reason (carotid ultrasound, CT, MRI)
* The importance of detection is the need to exclude thyroid cancer
132
What can cause thyroid nodules?
* non malignant thyroid nodules
* thyroid adenomas
- colloid nodules
- thyroid cysts
133
colloid nodules?
* colloid nodules - most common type of thyroid nodule - may develop due to cystic degeneration of thyroid tissue.
134
thyroid cysts?
* thyroid cysts - can develop from degeneration of thyroid tissue, retention of secretions within thyroid follicles, or hemorrhage into a pre-existing nodule.
* Thyroid cysts are usually benign.
135
Ix of thyroid nodules?
* Thyroid function tests (if abnormal suggest benign lesion) and autoantibodies
* Thyroid ultrasound and fine needle aspiration cytology (FNAC)
* Scintigraphy (thyroid isotope scan) – increased uptake more likely benign)
136
prophythiouracil (PTU)?
* choice of drug during T1 bc carbimazole can cause congenital malfirmation
* suppresses production of thyroid hormone and blocking peripheral conversion of T4 to T3
137
side effects of PTU?
hepatotoxicity
138
Risk of agranulocytosis w ?
* agranulocytosis w PTU and carbimazole
* if ppts develop sore throat or fever stop the medication
139
how long does carbimazole need to be taken for?
* 12-18 months
140
if there is recurrence of hyperthyroidism or develop neutropenia while on carbimazole:
* radioiodine therapy
* total thyroidectomy
141
Primary hypothyroidism?
* DYSFUNCTION OF THE THYROID GLANd
* INADEQUATE PRODUCTION OF THYROID HORMONES
142
Drugs that interfere w abs of thyroxine?
* ferrous sulphate
* calcium carbonate
* PPI
143
Drugs that increase turnover of thyroxine
* rifampicin
* phenytoin
* carbamazepine
144
how should levothyroxine be taken?
* empty stomach
* ensure no food or drink at least 30-60 mins after levothyroxine ingestion
145
congenital autoimmune disease association ?
* T1D
* autoimmune thyroid disorder
* addisons disease
* coeliac disease
146
Thyroxine is abs in?
* abs in small intestine
* max abs in first 2 hours of ingestion
* severe hypothyroidism itself can impair abs due to oedema of the SI
147
what is not a pre-requestie of thyrotoxicosis?
* Thyrotoxicosis: refers to an excess of thyroid hormone, having an overactive thyroid gland is not a prerequisite (e.g. ingestion of excess thyroid hormone).
* more commonly affects women than men - 5-10x more likely
148
TRH secretion?
* TRH is secreted from the paraventricular nucleus of the hypothalamus
149
TRH ->
* reaches the AP where it causes release of TSH
* Transported in the blood, TSH acts upon the thyroid gland promoting the synthesis and release of thyroid hormone.
150
TSH is produced by?
* TSH, produced by the thyrotrophs of the anterior pituitary, is released following stimulation by TRH.
151
Thyroid hormones negative feedback?
* These thyroid hormones complete a negative feedback loop through the suppression of TRH and TSH release.
152
what are the effects of T3/T4?
* Inc basal metabolic rate
* it has anabolic effects at low serum levels and catabolic effects at higher levels on metabolism
* increases release and effect of GH and IGF-1.
* increases the heart rate and contractility through increasing sensitivity to catecholamines.
153
What is the most common cause of thyrotoxicosis in the uK?
graves
154
What causes graves?
* It is caused by IgG antibodies to the TSH receptors found within the thyroid - thyroid-stimulating hormone receptor antibodies (TSHR-Ab),
* these antibodies mimic the action of TSH causing excessive stimulation of the gland.
155
Second most common cause of hyperthyrodiism?
toxic multinodar goitre
156
TMNG?
* multiple autonomous nodules develop that are capable of producing and secreting thyroid hormones.
157
solitary toxic adenoma?
single adenoma develops and produces and releases excess thyroid hormones.
`
158
amiodarone induced thyrotoxicosis?
* amiodarone has a high iodine content
* can cause hyper and hypothyroidism
159
type 1 amiodarone induced thyrotoxicosis?
* In type 1 the Jod-Basedow phenomenon, in which excess iodine intake causes excess thyroid hormone synthesis - seen in ppts w pre-existing thyroid disease
160
follicular thyroid cancer?
In metastatic follicular thyroid cancer, malignant tissue may remain functional. The increased amounts of tissue can lead to an overproduction of thyroid hormone.
161
Hyperthyroidism is caused by thyroid hormone release from ectopic thyroid tissue related to:
* Ovarian teratomas
* Dermoid tumours
* majority of these tumours are benign
162
beta-HCG related thyrotoxicosis?
Beta-HCG is thought to mimic the action of TSH causing thyroid hormone synthesis and release. It occurs in states of elevated Beta-HCG:
* Pregnancy
* Hydatidiform mole
* Choriocarcinoma
* Testicular germ cell tumour
163
secondary hyperthyroidism?
* characterised by excess TSH production -> inc T3/T4
* very rare
164
secondary hyperthyroidism is typically caused by?
TSH secreting pituitary adenoma
165
thyrotoxicosis without hyperthyroidism ?
* Thyroiditis: inflammation of the thyroid gland resulting in the release of stored thyroid hormone.
* Exogenous ingestion: a person ingests thyroid hormone.
166
supra-therapeutic doses of levothyroxine?
* When taken at supra-therapeutic doses levothyroxine may cause thyrotoxicosis without hyperthyroidism. Patients may abuse levothyroxine for weight-loss purposes.
167
De Quervain’s (subacute granulomatous) thyroiditis =
* self limiting
* viral in oirgin?
* results in inflammation of the thyroid gland and release of thyroid hormone.
168
classical feature of De Quervain's thyroiditis?
painful goitre
169
3 phases of De Quervains thyroiditis?
* Thyrotoxicosis
* Hypothyroidism
* Resolution
170
amiodarone induced type 2?
Type 2 is caused by a destructive thyroiditis with resultant release of thyroid hormone.
171
what can hyperthyroidism cause in men?
gynaecomastia
172
signs of hyperthyroidism?
* Goitre
* Sinus tachycardia/arrhythmias
* Hair loss
* Palmar erythema
* Tremor
* Thyroid bruit (Graves’)
* Myxoedema - deposition of mucopolysaccharides in the skin leading to swelling.
173
Graces opthamology?
* graves opthmology
* more commonly seen in smokers
* Inflammation and accumulation of mucopolysaccharides occur in the retro-orbital adipose tissue and extra-ocular muscles.
174
what inc risk of graves opthamology?
radioiodine
175
features of graves opthamology?
* Features include proptosis, periorbital oedema, lid retraction, eye pain and visual loss.
176
thyroid dermopathy?
* most common manifestation is pretibial myxoedema.
* This is an infiltrative dermopathy resulting from deposition of mucopolysaccharides in the dermis.
177
thyroid acropachy?
* This is characterised by periostitis, nail clubbing and soft tissue swelling of the extremities.
* It's most commonly seen in smokers with co-concomitant Graves’ ophthalmopathy
178
T3 and T4 - conversion?
Though T3 is more biologically active than its counterpart T4, secreted thyroid hormone is 90% T4. Peripherally much of T4 is converted to T3.
179
Blood results in primary hyperthyroidism?
- low TSH
- raised T4 and T3
180
Blood results of secondary hyperthyroidism?
- e.g. pituitary adenoma
- high TSH and raised T3 and T4
181
Sublinical hyperthyroidism?
low TSH with a normal fT4 and fT3.
182
autoab in graves?
Thyroid-stimulating hormone receptor antibodies (TSHR-Ab) are seen in > 90% of those with Graves’ disease.
183
Imaging for hyperthyroidism?
* Ultrasonography
* Thyroid uptake scan
184
# Thyrotoxicosis
Thyroid uptake scan?
* Thyrotoxicosis with increased uptake: indicative of increased hormone synthesis
* Thyrotoxicosis with decreased uptake: indicative of inflammation/destruction of the thyroid gland with the release of thyroid hormone
185
Initial therapy for hyperthyroidism?
* Following diagnosis, patients are normally offered thioamides (carbimazole or propylthiouracil) whilst a decision on definitive therapy is being made.
* Definitive therapy may be radioactive iodine, ongoing thioamide therapy or surgery.
186
symptomatic relief of hyperthyroidism?
* A beta-blocker or calcium channel blocker may be prescribed to treat adrenergic symptoms whilst the thioamides take effect.
187
radioactive iodine?
Iodine is key to the synthesis of thyroid hormones. As such when radioactive iodine (RAI) is given it is taken up by the thyroid causing destruction and reduced thyroid hormone release.
188
CI for radioactive iodine?
* Current pregnancy
* Falling pregnant within 6 months of treatment
* Breastfeeding
* Fathering a child within 4-6 months of treatment
189
cautions w radioactive iodine?
* For a short time following treatment, the patient will emit some radiation.
* As such they will be advised to avoid close contact with members of their household and restrict any contact with children or pregnant women for several weeks.
190
which ppts are offered radioactive iodine first line?
* Typically offered first line in graves in those suitable and not likely to enter remission
* It is often offered as first-line definitive management for toxic multinodular goitre.
191
what may RAI aggrevate in graves?
can exacerbate or cause opthamology
192
Propylthiouracil can be considered in adults where the patient is/has:
* Intolerant/allergic to carbimazole
* Pregnant or planning on pregnancy in the next 6 months
* A history of pancreatitis
193
What are the thionamides?
- carbimazole
- PTU
194
Baselines before thionamides are started?
* Baseline FBC and LFTs are obtained prior to the commencement of thioamides.
195
what is a CI of thionamides?
* Neutropenia or severely deranged transaminases are a contraindication to treatment.
196
thyroidectomy?
* may be used as definitive therapy if malignancy is suspected, there is a compressive goitre or RAI/ anti-thyroid medications are unsuitable.
* Hemithyroidectomy (removal of half the thyroid gland) may be offered to patients with a solitary toxic nodule.
197
complications of thyroidectomy?
- hypocalcaemia
- recurrent laryngeal nerve injury
198
hypocalcaemia after thyroidectomy?
* hypocalcaemia - typically transient, may be permanent in a minority of cases. Due to the proximity of the parathyroid glands to the thyroid gland.
199
recurrent LN injury after thyroidectomy?
* Recurrent laryngeal nerve injury: presents with hoarse voice post-operatively.
200
thyrotoxic crisis may result from...
* may result from decompensation during an illness
201
how does thyrotoxic crisis present?
- hyperthermia
- tachycardia
- arrhythmia
- nausea
- vomiting
- seizures
- cognitive decline
202
Mx of thyrotoxic crisis?
- BBs
- thionamides
- corticosteroids
- Lugol's iodine
tommy went to C a BTL
203
Corticosteroids in thyrotoxic crisis?
reduced conversion of T4 to T3
204
thyroid replacement therapy - prescription?
* Advise the person to take LT4 medication on an empty stomach in the morning before other food or medication.
205
Features of thyroid cancer?
* Thyroid nodule/mass
* Hoarseness/ change in voice
* Cervical lymphadenopathy
* Stridor
- painless goitre
206
Stridor =
harsh, high pitched sound, normally heard on inspiration, indicative of upper airway obstruction
207
Features of thyroid malignancy on US?
* Microcalcifications
* Hypoechongenicity
* Irregular margin
* Increased vascularity
208
Hypothyroidism - primary?
* Primary hypothyroidism (overt): Elevated thyroid stimulating hormone (TSH) levels (typically > 10 mU/L) with a free T4 (fT4) level below the normal range.
209
Subclinical hypothyroidism?
* Subclinical hypothyroidism: The subclinical state is characterised by elevated TSH levels but T3/T4 that remains within the normal range
210
secondary hypo?
* disease/ damage to pituitary which reduces production of TSH
* most frequently caused by pituitary adenomas.
* reduced levels of thyroid hormone accompanied by reduced TSH (due to lack of production).
211
tertiary hypo?
* disease or damage to the hypothalamus or the hypophyseal portal system may reduce the production, release or transport of TRH.
* we expect to find reduced levels of thyroid hormone accompanied by reduced TSH and TRH.
212
Resistance to thyroid hormone?
* inherited disorder is caused by an unresponsive form of one of the T3 receptors.
* It is characterised by raised levels of thyroid hormone and TSH (as negative feedback is somewhat inhibited by hormone resistance).
* This compensatory increase means most individuals are clinically euthyroid.
213
what happens in hashimotos?
* ab mediated destruction of thyroid
214
2 forms of hashimotos?
* Goitrous: characterised by a firm and rubbery goitre
* Atrophic: characterised by an atrophic gland
215
epidemiology of hashimotos?
* more freq seen in women
* becomes inc common w age
216
what is hashimotos assoc w ?
* assoc w T1D, turners and downs syndrome
217
what is the leading cause of hypothyroidism?
- worldwide: iodine def
- in the UK, hashimotos
218
Amiodarone induced hypo - Wolff Chaikoff effect?
* Pre-existing autoimmune disease: hypothyroidism may occur secondary to the Wolff–Chaikoff effect - a phenomenon in which raised iodine intake results in reduced levels of thyroid hormone.
219
Amiodarone induced hypothyroidism - normal thyroid gland?
those with a normal gland may also develop hypothyroidism, frequently affecting T3.
220
congenital hypothyroidism?
* screened for with the Guthrie screen to prevent cretinism (the syndrome caused by congenital hypothyroidism). It may be due to:
* Dyshormonogenesis
* Abnormal gland development
221
symptoms of hypo?
* Tiredness
* Lethargy
* Weight gain
* Cold intolerance
* Reduced libido
* Goitre
222
menstrual changes in hypo?
* Menstrual irregularities (oligomenorrhoea, amenorrhoea, menorrhagia)
- everything gets heavy so periods get heavy
223
signs of hypo?
* Hair loss (characteristically the outer third of the eyebrows)
* Dry skin
* Goitre
* Bradycardia
* Myxoedema
* Delayed relaxation phase of deep tendon reflexes
224
Primary hypothyroidism =
raised TSH and reduced fT4.
225
secondary/ tertiary hypo blood results =
normal (inappropriately normal) or lowered TSH or TRH and a reduced fT4.
226
subclinical hypothyroidism?
* Subclinical hypothyroidism refers to a raised TSH but normal fT4.
227
Autoab in hashimotos?
* Anti-TPO - hashimotos but can also be seen in graves
* anti-Tg - hashimotos commonly
228
TSHR-ab?
* TSHR-ab - graves but can also be seen in hashimotos where they block TSh receptors preventing their activation
229
other tests for hypo?
* FBC
* B12 and Folate
* Serum lipids
* HbA1c
* Coeliac serology
230
suspicion of malignancy ->
* Ultrasonography
* Specialist referral (urgent two week wait)
231
Ix of hypothyroidism?
* levothyroxine
* TSH levels are checked every 2-3 months then yearly once stable
232
myxodema coma often results from?
- acute decompensation during an illness
233
how do ppts w myexoedema coma present?
- hypotension
- hypothermia
- bradycardia
- cognitive decline
234
Myxoedema coma Tx?
Myxoedema coma is a medical emergency requiring treatment with:
-**** IV thyroid replacement
- IV fluid
- IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded)****
- electrolyte imbalance correction
- sometimes rewarming
235
Diagnosis of adrenal insufficiency involves?
- random cortisol
- 9am cortisol
- short syncathen/ ACTH stimulation test
236
9am cortisol?
* 9am cortisol - cortisol levels highest in the morning
* <100 nmol confirms adrenal insufficiency
237
what is the definitive test for adrenal insufficiency?
* Short synacthen /ACTH stimulation test (definitive test)
238
short synacthen test?
* normal resp is 30 min cortisol >550mmol/L
* tests response to synthetic ACTH - how much cortisol is produced?
239
primary vs secondary adrenal insufficiency?
- primary adrenal insufficiency: defect within the adrenal gland
- seconday adrenal insufficiency: defect in pituitary/ hypothalamus (ACTH/ CRH)
240
acute management of P adrenal insufficiency?
* Fluids: 1-3L of 0.9% Saline
* Hypoglycaemia: iv dextrose
* Glucocorticoids: Hydrocortisone
241
LTM of P adrenal insufficiency?
* hydrocortisone 3x day
* fludocortisone once daily to replace aldosterone
* ? androgen replacement
242
sick day rules?
*Never stop steroids
*Double dose during illness/infection
*If unable to take PO Hydrocortisone, need IM/IV Hydrocortisone
*Carry steroid card / MedicAlert bracelet
243
diagnosis of secondary AI?
* deficiency of ACTH - no obv cause -> image pituitary
* Failed SST
* ACTH low or suppressed
* History of exogenous steroid use
244
CP of secondary adrenal insufficiency?
* no hyperpigmentation - ACTH is low/ normal
* no dehydration or hyperkalaemia - aldosterone intact
* hypoglycaemia more common
* clinical manifestations of tumour
245
LTM of secondary adrenal insuffiency?
* Hydrocortisone replacement
* No need for Fludrocortisone
* Taper steroids gradually
* sick day rules
246
management of secondary vs primary AI?
- primary: hydrocortisone + fludorcortisone
- secondary: just hydrocortisone no fludro
247
what happens in addisons disease?
Primary adrenal insufficiency (Addison's disease): caused by destruction or dysfunction of the adrenal cortex
248
what happens in SAI?
- caused by a reduction in ACTH release
- May be seen as part of panhypopituitarism, an isolated deficiency, following brain injury or secondary to medications.
249
TAI?
Tertiary adrenal insufficiency: caused by a reduction in corticotropin-releasing hormone, most commonly seen following chronic glucocorticoid steroid use.
250
symptoms of AI - loss of glucocorticoid and mineralcorticoid function?
* loss of normal glucocorticoid and mineralcorticoid function -> dehydration, weight loss, abd pain, nausea, vomiting, mood dist
251
features of AI in women?
* In women features of androgen deficiency - including loss of libido and hair loss in the axilla/pubic region - may be seen
* This rarely affects men where the testes are the primary site of androgen production
252
addisonian crisis?
* addisonian crisis: medical emergency caused by profound glucocorticoid and mineralocorticoid deficiency that may be triggered by intercurrent illness.
253
zones of the adrenal cortex?
- zona glomerulasa
- zona fasiculata
- zona reticularis
254
zona glomerulasa?
mineralocorticoids - aldosterone is the key mineralocorticoid, release primarily controlled by the renin-angiotensin system
255
zona fasiculata?
glucocorticoids - release controlled by hypothalamic-pituitary-adrenal axis
256
zona reticularis?
androgens - produces dehydroepiandrosterone (DHEA).
257
adrenal medulla produces?
* Adrenaline
* Noradrenaline
* Dopamine
258
CRH is released from?
paraventricular nucleus of the hypothalamus.
259
CRH ->
* stimulates ACTH release from anterior pituitary
* ATCH -> cortisol from adrenal cortex
* cortisol exerts negative feedback on release of both ACTH and CRH
260
Aldosterone?
* released from zona glomerulasa of adrenal cortex
* in response to: A2, ACTH, potassium levels
261
aetiology of addisons - most common cause worldwide?
* worldwide most common cause is TB
262
most common cause of addisons in the west?
autoimmune adrenalitis
263
other causes of addisons?
* HIV
* disseminated fungal infections
* syphilis
* malignant mets
* amyloid deposits
* bilateral adrenalectomy is iatrogenic
264
how do ppts w addiosn tend to present?
* majority of patients present w a chronic, insidious onset
* Features may be vague and non-specific with patients complaining of fatigue, anorexia and abdominal pain
265
features of addisons in women?
* in women, androgen deficiency: loss of libido, loss of hair in axillary/ pubic regions
266
what is spec to PAI?
* hyperpigmentation - mucous membranes and palmar creases
267
Signs of addisons
268
# When is it most commonly seen?
addisonian crisis is caused by?
* caused by a significant deficiency in glucocorticoids and mineralocorticoids.
* It is most commonly seen in tertiary adrenal insufficiency (termed an 'adrenal crisis') as a result of the sudden withdrawal of exogenous steroids.
269
addisonian crisis from addisons?
* in addisons, can occur following an acute decompensation where an additional stress (e.g. infection) results in an exacerbation of a pre-existing deficiency
* . Bilateral adrenal gland haemorrhage can also result in a crisis.
270
symptoms of addisonian crisis?
* dehydration, hypotension and confusion, coma, pyrexia, shock, hyperpig
* Blood tests may reveal hyponatraemia, hyperkalaemia and hypoglycaemia.
271
addisons: aldosterone def ->
hyponatreamia and hyperkalamia
272
Blood tests for AI?
* morning cortisol < 100 - means AI very likely
* 100-500 - AI possible
* > 500 AI unlikely
273
distinguishing between types of AI?
* plasma ACTH
* High: indicative of Addison's disease (primary adrenal insufficiency)
* Low: indicative of secondary/tertiary adrenal insufficiency
274
short synacthen test?
* Cortisol is measured at three time points: 0 (i.e. immediately before), 30 and 60 minutes following administration. The test is carried out in the morning, normally commencing at 8 am.
* The baseline reading of cortisol should be >180-190 nanomol/L.
* Serum cortisol > 500–550 nanomol/L either before or following the ACTH is considered normal.
275
Mx of addisons?
* glucocorticoid replacement: hydrocortisone
* mineralcorticoid replacement: fludocortisone
* androgen replacement
276
Mx of addisonian crisis?
* IV hydrocortisone
* IV fluid rehydration
277
secondary AI?
* inadequate ACTH -> adrenal glands not stim -> low cortisol
* result of loss/ damage to pituitary gland
278
What can lead to SAI?
* Tumours (e.g., pituitary adenomas)
* Surgery to the pituitary
* Radiotherapy
* Sheehan’s syndrome
* Trauma
279
Sheehan's syndrome?
where major post- partum haemorrhage causes avascular necrosis of the pituitary gland )
280
TAI?
* inadequate CRH from hypothalamus
* usually from use of long term oral steroids - for more than 3 weeks causing suppression of the hypothalamus via negative feedback
281
Pathophys of TAI?
* When the exogenous steroids (originating outside the body) are suddenly withdrawn, the hypothalamus does not “wake up” fast enough, and endogenous steroids (originating inside the body) are not adequately produced.
* Therefore, long-term steroids must be tapered slowly to allow the adrenal axis to regain normal function.
282
symptoms of AI?
* Fatigue
* Muscle weakness
* Muscle cramps
* Dizziness and fainting
* Thirst and craving salt
* Weight loss
* Abdominal pain
* Depression
* Reduced libido
283
primary AI - skin?
* Bronze hyperpigmentation of the skin, particularly in creases (ACTH stimulates melanocytes to produce melanin) - PRIMARY
284
? ? is a sign of AI
* Hypotension (particularly postural hypotension – with a drop of more than 20 mmHg on standing)
285
Autoantibodies may be present in autoimmune adrenal insufficiency:
* Adrenal cortex antibodies
* 21-hydroxylase antibodies
286
Year 3
flashcards
Decks in class (45)
# Cards
-
Clinical Skills256
-
Block 32 Week 172
-
Block 32 Week 2247
-
Block 32 Week 3&4266
-
Block 32 Week 4317
-
Block 32 Week 5274
-
Block 32 Week 7&8291
-
Block 31 Week 1318
-
Block 31 Week 2295
-
Block 31 Week 3232
-
Block 31 Week 4266
-
Block 31 Week 5241
-
Block 31 Week 6238
-
Block 31 Week 7216
-
Block 31 Week 8244
-
Block 31 Pharmacology261
-
Block 31 PPT205
-
Block 31 H&S222
-
Block 32 H&S411
-
Block 32 PPT200
-
Block 33 Week 1254
-
Block 33 Week 2283
-
Block 33 H&S554
-
block 33 week 3201
-
Block 33 Week 4241
-
Block 33 Week 5281
-
Block 33 Week 6243
-
Block 33 Pharmacology149
-
Block 33 Week 7212
-
Block 33 Week 8235
-
Block 33 H&S251
-
Block 34 Week 1237
-
Block 34 Week 2224
-
block 34 week 3270
-
Block 34 Week 4286
-
Block 33 PPT334
-
Block 32 Pharm190
-
Block 34 Week 5252
-
Block 34 Week 6279
-
Block 34 H&S384
-
Block 34 Week 8345
-
Block 34 Week 7262
-
Block 34 PPT319
-
Block 34 Pharm381
-
Block 32 Week 8287
