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Year 3 > Block 34 Week 4 > Flashcards

Block 34 Week 4 Flashcards

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
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2
Q

self monitoring w t1?

A
  • at least 4x a day
  • before each meal and before bed
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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.
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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
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5
Q

first line in diabetics w HTN ?

A

ACEi - renoprotective effects

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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
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7
Q

primary care in diabetes Mx?

A
  • services include regular monitoring, diabetic education, lifestyle advice, and medication management
  • GPs, practice nurses, dietitians
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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.
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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
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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.
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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
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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.
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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.
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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.
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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.
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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
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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,
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18
Q

Symptoms of T1D?

A
  • Polyuria & polydipsia
  • Weight loss
  • Vomiting
  • Lethargy
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19
Q

signs of T1D?

A
  • Mild-moderate dehydration (dry skin, dry mucous membranes, reduced skin turgor)
  • BMI < 25
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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
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21
Q

signs of DKA?

A
  • Shock(tachycardia, hypotension)
  • Kussmaul breathing(Deep sighing respiration)
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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)
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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).

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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.
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25
Q

biphasic regime of insulin?

A
  • 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.
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26
Q

cont insulin infusion?

A
  • 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.
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27
Q

monitoring for complications of diabetes?

A
  • 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
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28
Q

diabetic foot?

A
  • Diabetic foot complications arise from a combination of neuropathy, PAD, and impaired wound healing.
  • They can result in foot ulcers, infections, and ultimately, amputations.
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29
Q

management of diabetic foot?

A
  • Proper foot care, early detection and treatment of ulcers, and multidisciplinary care are crucial to preventing severe outcomes.
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30
Q

diabetic nephropathy?

A
  • diabetic nephropathy
  • characterized by albuminuria, declining glomerular filtration rate (GFR), and eventually, renal failure
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31
Q

Management of diabetic nephropathy?

A

ACE or ARB used

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32
Q

insulin adjuncts - when should metformin ve added in T1D?

A
  • they have a BMI of 25kg/m2or above (23kg/m2or 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.
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33
Q

What is obesity?

A
  • disease when excessive body fat results in pathogenic structural or functional abn resulting in increased ppt morbitiy and mortality
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34
Q

advantages of using BMI?

A
  • 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
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35
Q

Disadvantages of using BMI?

A
  • 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
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36
Q

obesity - history:

A

image

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37
Q

physical exam for obesity

A

vital signs

  • Waist circumference
  • neck circumference
  • height and weight
  • BP
  • pulse
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38
Q

nutritional therapy for obesity?

A
  • very low calorie diets
  • reduces glucose, insulin
  • reduces bp
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39
Q

risks of obesity?

A
  • cold intolerance, dysmenorrhea
  • faigue, hair loss, brittle nails
  • small inc in gallstones, kidney stones and gout flare
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40
Q

exercise prescription (FITTE)

A
  • frequency
  • intensity
  • time spent
  • type
  • enjoyment level
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41
Q

Meds for obesity?

A
  • Orlistat: lipase inhibitor
  • liraglutide: GLP-1 analogue
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42
Q

indications

Bariatric surgery for obesity?

A
  • BMI of >35 with >1 AHC
  • BMI of > 40 w or without AHC
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43
Q

dietary recommendations for obesity?

A
  • 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)
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44
Q

Weight gain occurs when there’s an imbalance in?

A
  • energy imbalance - Weight gain occurs when energy intake (calories consumed) exceeds energy expenditure (calories burned
  • high calorie food and sedentary lifestyle
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45
Q

weight gain - environment?

A
  • 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.
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46
Q

SE factors in weight gain?

A
  • SE factors - individuals from lower-income households facing greater barriers to accessing healthy foods, safe recreational spaces, and healthcare service
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47
Q

food deserts and weight gain?

A
  • 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.
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48
Q

psychological factors in weight gain?

A
  • psychological factors - stress, depression, anxiety, and emotional eating, can influence eating behaviors and contribute to weight gain.
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49
Q

coping mechanisms & weight gain?

A
  • Unhealthy coping mechanisms, such as using food as a reward or comfort, and maladaptive dietary patterns, such as binge eating or night eatin
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50
Q

cultural and social norms in weight gain?

A
  • cultural and social norms - Cultural celebrations, social gatherings, and food-centric traditions may promote overeating and contribute to weight gain in Western societies.
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51
Q

Why is prev of obesity inc in western society?

A
  • 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
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52
Q

Social implications of obesity?

A
  • 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
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53
Q

social impacts of obesity - healthcare disparities?

A
  • 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.
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54
Q

physical implications of obesity?

A
  • 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.
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55
Q

economic impacts of obesity - healthcate?

A
  • 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
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56
Q

economic impacts of obesity?

A
  • Productivity loss
  • disability payments
  • economic disparities
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57
Q

economic disparities and obesity?

A
  • economic disparities - Obesity disproportionately affects socioeconomically disadvantaged populations, exacerbating existing inequalities in access to healthcare, education, employment opportunities, and healthy food options
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58
Q

what are the population impacts of obesity?

A
  • public health burden
  • reduced life expectancy
  • socioeconomic disparities
  • interconnected health risks
  • childhood obesity epidemic
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59
Q

Strategies for reducing obesity - info?

A
  • 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.
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60
Q

strategies for reducing obesity - envir change?

A
  • 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.
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61
Q

strategies for reducing obesity - partnerships?

A
  • 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.
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62
Q

Behavioural interventions of obesity?

A
  • 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
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63
Q

Physical activity in order to manage obesity?

A
  • to avoid obesity people may need to do 45 to 60minutes 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 90minutes of activity a day to avoid regaining weight
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64
Q

use when

Liraglutide?

A
  • 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
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65
Q

side effects of liraglutide?

A
  • gallstone disorders
  • vomiting
  • acute pancreatitis
  • diarrhoea
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66
Q

used when

orlistat?

A
  • BMI of 30+
  • or 28+ with more RF
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67
Q

side effects of orlistat?

A
  • abd pain - may be minimised by reduced fat intake
  • anx
  • diarrhoea
  • GI disorders
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68
Q

used when?

semaglutide?

A
  • at least 35
  • Lower BMI thresholds for people from South Asian, Chinese, other Asian, Middle Eastern, Black African or African-Caribbean family backgrounds
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69
Q

side effects of semaglutide?

A
  • cholelithiasis
  • GI disorders
  • hypoglycaemia
  • weight decreased & appetite dec
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70
Q

Indications

surgical interventions for obesity?

A
  • 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
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71
Q

types of bariatic surgery?

A
  • laparoscopic adjustable gastric banding
  • sleeve gastrectomy
  • Roux-en gastric bypass
  • billiopancreatic diversion
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72
Q

Laparoscopic adjustable gastric banding (LAGB)?

A
  • 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
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73
Q

What is the safest and least invasive type of bariatic surgery?

A

LABG

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74
Q

LABG - weight loss peaks at?

A

18 months post-procedure

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75
Q

LABG -

A
  • Can make some foods difficult to tolerate
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76
Q

LABG - band related complications?

A

Slippage, erosion, or leakage of the gastric band, which may require surgical revision or removal.

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77
Q

LABG - band intolerance?

A

Some individuals may experience discomfort, pain, or intolerance to the gastric band, leading to inadequate weight loss or complications.

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78
Q

sleeve gastrectomy?

A
  • 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
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79
Q

what is required after a sleeve gastrectomy?

A
  • Patients require mulitvitamin, and sometimes iron and B12 supplementation for life
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80
Q

risks of sleeve gastrectomies?

A
  • acid reflux
  • strictures
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81
Q

Acid reflux after a sleeve gastrectomy?

A
  • Acid reflux: Increased risk of gastroesophageal reflux disease (GERD) due to changes in stomach anatomy and increased pressure on the lower esophageal sphincter.
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82
Q

Strictures after a sleeve gastrecomy?

A
  • Strictures: Narrowing of the stomach opening or sleeve, which can cause difficulty swallowing and may require further treatment or intervention.
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83
Q

Roux-en-Y gastric bypass?

A
  • 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
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84
Q

considerations of RYGB?

A
  • Multivitamin supplementation required for life
  • dumping syndrome
  • nutrional deficiencies - vitamin B12, iron, calcium, folate
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85
Q

biliopancreatic diversion?

A
  • 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
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86
Q

side effect of bilipancreatic diversion?

A
  • Foul-smelling stools and flatulence: Changes in digestion and absorption patterns can lead to unpleasant digestive symptoms.
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87
Q

Dumping syndrome?

A

Dumping syndrome describes a group of symptoms caused byfood rapidly emptyingor being ‘dumped’ from thestomach into the small intestines. This results in undigested food within the small intestine that the body finds difficult to absorb.

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88
Q

symptoms of dumping syndrome?

A

sweating, bloating, abdominal cramps/pain, diarrhoea, and nausea.

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89
Q

Relationship between impaired glucose tolerance and obesity?

A
  • excess body fat, especially abdmonal can lead to insulin resistance -> hyperglaemia -> development of impaired glucose tolerance -> T2DM
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90
Q

Diabetes prevention programme trial found that?

A
  • 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
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91
Q

NHS diabetes prevention programme?

A
  • 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
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92
Q

Anatomy of the thyroid?

A
  • Comprises 2 lobes connected by an isthmus
  • Usually palpable and moves with swallowing
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93
Q

physiology of thyroid hormones?

A
  • 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
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94
Q

Hyperthyroidism?

A

*Excess thyroid hormone production by the thyroid gland

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95
Q

thyrotoxicosis=

A

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

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96
Q

causes of hyperthyroidism?

A

o Grave’s disease
o Multinodular goitre
o Single functioning nodule
o Thyroiditis, including post partum thyroiditis
o Drugs

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97
Q

2 main causes of hyperthyroidism?

A

graves disease and nodular thyroid disease

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98
Q

Graves disease epidemiology?

A
  • younger age
  • 10x more prev in females
  • often familial
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99
Q

causes of graves disease?

A
  • Autoimmune disorder (positive thyroid antibodies - TPO and TSH receptor Ab)
  • May be self limiting
  • Thyrotoxicosis may be severe
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100
Q

nodular thyroid disease affects?

A
  • older age
  • equal gender ratio
  • Rarely familial
  • No autoantibodies
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101
Q

nodular thyroid disease - onset?

A
  • Gradual onset
  • Persistent
  • Usually mild
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102
Q

symptoms of hyperthyroidism?

A
  • anxiety
  • emotional lability
  • weakness
  • tremor
  • palpitations
  • heat intolerance, excessive sweating
  • diarrhoea
  • increased perspiration
  • weight loss despite a normal or increased appetite
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103
Q

signs of hyperthyroidism in females?

A
  • female: amenorrhoea or oligomenorrhea
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104
Q

Eye signs in hyperthyroidism

A
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105
Q

exophthalmos

A

IMAGE

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106
Q

clinical signs in thyrotoxicosis - speech?

A
  • Rapid speech, agitation
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107
Q

clinical signs of thyrotoxicosis - eyes?

A
  • Eyes – lid retraction and lag (sympathetic overactivity),
  • orbital inflamation (Graves disease)
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108
Q

Skin signs of graves?

A
  • Skin – warm and moist, pre-tibial myxoedema (Graves disease)
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109
Q

pre-tibial myxoedema?

A

skin condition that causes plaques of thick, scaly skin and swelling of your lower legs

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110
Q

pulse in HT?

A
  • Pulse – tachycardia or atrial fibrillation
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111
Q

NM signs of thyrotoxicosis?

A
  • Neuromuscular – tremor, proximal muscle weakness
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112
Q

neck signs of hyperthyroidism?

A
  • Neck – presence and size of goitre depends on cause
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113
Q

how may old ppl w hyperthyroidism present?

A
  • Older people may present with only weight loss or symptoms of heart failure
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114
Q

lab results for hyperthyroidism?

A
  • raised thyroid hormones - usually T3 and T4 but may be only one or the other
  • TSH usually suppressed below detection limit
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115
Q

ab in hyperthyroidism?

A
  • Thyroid peroxidase antibodies and TSH receptor antibodies
116
Q

thyroid eye disease

A
  • 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
Q

Medical Tx of hyperthyroidism?

A

1) carbimazole
2) propylthiouracil - first trimester

118
Q

surgical therapy for hyperthyrodisim?

A

partial or total thyroidectomy

119
Q

what is given for symptomatic relief for hyperthyrodism?

A

BB - propanol

120
Q

radiotherapy in hyperthyroidism?

A

radioactive iodine

121
Q

hypothyroidism?

A
  • most in common females
  • Most common form is primary hypothyroidism, but can also be secondary hypothyroidism (hypothalamopituitary failure)
122
Q

lab tests in hypothyroidism?

A

*Raised TSH
*Reduced FT4 and FT3
*Thyroid peroxidase antibodies (TPO) usually positive in autoimmune disease

123
Q

causes of hypothyroidism?

A

* Autoimmune (Hashimoto’s thyroiditis)
* Iatrogenic (surgery, radioiodine treatment)
* Drugs e.g.
* Directly causing hypothyroidism
* Affecting hormone metabolism
* Affecting gastrointestinal absorption

124
Q

Symptoms of hypothyroidism - slowing of metabolic processes?

A

cold intolerance, fatigue, weight gain etc

125
Q

hypothyroidism symptoms - tissue deposition?

A
  • tissue deposition of matrix glycosaminoglycans – skin changes, hoarse voice, tongue enlargement etc
126
Q

Extremes of thyroid dysfunction?

A
  • Myxoedema coma – extreme hypothyroidism
  • Thyroid storm – extreme thyrotoxicosis
  • Both have high mortality
127
Q

Tx of hypothyroidism?

A
  • levothyroxine
  • lifelong
128
Q

goitre =

A

*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
Q

Ix for a goitre?

A

o Fine needle aspiration
o Ultrasound
o Radionucleotide imaging
o Computed tomography/MRI

130
Q

Most common symptoms of a substernal goitre?

A
  • wheeze
  • dyspnoea
  • cough
131
Q

thyroid nodules are usually noticed when?

A
  • 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
Q

What can cause thyroid nodules?

A
  • non malignant thyroid nodules
  • thyroid adenomas
  • colloid nodules
  • thyroid cysts
133
Q

colloid nodules?

A
  • colloid nodules - most common type of thyroid nodule - may develop due to cystic degeneration of thyroid tissue.
134
Q

thyroid cysts?

A
  • 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
Q

Ix of thyroid nodules?

A
  • 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
Q

prophythiouracil (PTU)?

A
  • 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
Q

side effects of PTU?

A

hepatotoxicity

138
Q

Risk of agranulocytosis w ?

A
  • agranulocytosis w PTU and carbimazole
  • if ppts develop sore throat or fever stop the medication
139
Q

how long does carbimazole need to be taken for?

A
  • 12-18 months
140
Q

if there is recurrence of hyperthyroidism or develop neutropenia while on carbimazole:

A
  • radioiodine therapy
  • total thyroidectomy
141
Q

Primary hypothyroidism?

A
  • DYSFUNCTION OF THE THYROID GLANd
  • INADEQUATE PRODUCTION OF THYROID HORMONES
142
Q

Drugs that interfere w abs of thyroxine?

A
  • ferrous sulphate
  • calcium carbonate
  • PPI
143
Q

Drugs that increase turnover of thyroxine

A
  • rifampicin
  • phenytoin
  • carbamazepine
144
Q

how should levothyroxine be taken?

A
  • empty stomach
  • ensure no food or drink at least 30-60 mins after levothyroxine ingestion
145
Q

congenital autoimmune disease association ?

A
  • T1D
  • autoimmune thyroid disorder
  • addisons disease
  • coeliac disease
146
Q

Thyroxine is abs in?

A
  • 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
Q

what is not a pre-requestie of thyrotoxicosis?

A
  • 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
Q

TRH secretion?

A
  • TRH is secreted from the paraventricular nucleus of the hypothalamus
149
Q

TRH ->

A
  • 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
Q

TSH is produced by?

A
  • TSH, produced by the thyrotrophs of the anterior pituitary, is released following stimulation by TRH.
151
Q

Thyroid hormones negative feedback?

A
  • These thyroid hormones complete a negative feedback loopthrough the suppression of TRH and TSH release.
152
Q

what are the effects of T3/T4?

A
  • 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
Q

What is the most common cause of thyrotoxicosis in the uK?

154
Q

What causes graves?

A
  • 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
Q

Second most common cause of hyperthyrodiism?

A

toxic multinodar goitre

156
Q

TMNG?

A
  • multiple autonomous nodules develop that are capable of producing and secreting thyroid hormones.
157
Q

solitary toxic adenoma?

A

single adenoma develops and produces and releases excess thyroid hormones.
`

158
Q

amiodarone induced thyrotoxicosis?

A
  • amiodarone has a high iodine content
  • can cause hyper and hypothyroidism
159
Q

type 1 amiodarone induced thyrotoxicosis?

A
  • 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
Q

follicular thyroid cancer?

A

In metastatic follicular thyroid cancer, malignant tissue may remain functional. The increased amounts of tissue can lead to an overproduction of thyroid hormone.

161
Q

Hyperthyroidism is caused by thyroid hormone release from ectopic thyroid tissue related to:

A
  • Ovarian teratomas
  • Dermoid tumours
  • majority of these tumours are benign
162
Q

beta-HCG related thyrotoxicosis?

A

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
Q

secondary hyperthyroidism?

A
  • characterised by excess TSH production -> inc T3/T4
  • very rare
164
Q

secondary hyperthyroidism is typically caused by?

A

TSH secreting pituitary adenoma

165
Q

thyrotoxicosis without hyperthyroidism ?

A
  • Thyroiditis: inflammation of the thyroid gland resulting in the release of stored thyroid hormone.
  • Exogenous ingestion: a person ingests thyroid hormone.
166
Q

supra-therapeutic doses of levothyroxine?

A
  • When taken at supra-therapeutic doses levothyroxine may cause thyrotoxicosis without hyperthyroidism. Patients may abuse levothyroxine for weight-loss purposes.
167
Q

De Quervain’s (subacute granulomatous) thyroiditis =

A
  • self limiting
  • viral in oirgin?
  • results in inflammation of the thyroid gland and release of thyroid hormone.
168
Q

classical feature of De Quervain’s thyroiditis?

A

painful goitre

169
Q

3 phases of De Quervains thyroiditis?

A
  • Thyrotoxicosis
  • Hypothyroidism
  • Resolution
170
Q

amiodarone induced type 2?

A

Type 2 is caused by a destructive thyroiditis with resultant release of thyroid hormone.

171
Q

what can hyperthyroidism cause in men?

A

gynaecomastia

172
Q

signs of hyperthyroidism?

A
  • Goitre
  • Sinus tachycardia/arrhythmias
  • Hair loss
  • Palmar erythema
  • Tremor
  • Thyroid bruit(Graves’)
  • Myxoedema- deposition of mucopolysaccharides in the skin leading to swelling.
173
Q

Graces opthamology?

A
  • graves opthmology
  • more commonly seen in smokers
  • Inflammation and accumulation of mucopolysaccharidesoccur in the retro-orbital adipose tissue and extra-ocular muscles.
174
Q

what inc risk of graves opthamology?

A

radioiodine

175
Q

features of graves opthamology?

A
  • Features include proptosis, periorbital oedema, lid retraction, eye pain and visual loss.
176
Q

thyroid dermopathy?

A
  • most common manifestation ispretibial myxoedema.
  • This is an infiltrative dermopathy resulting from deposition of mucopolysaccharides in the dermis.
177
Q

thyroid acropachy?

A
  • This is characterised by periostitis, nail clubbing and soft tissue swellingof the extremities.
  • It’s most commonly seen in smokers with co-concomitant Graves’ ophthalmopathy
178
Q

T3 and T4 - conversion?

A

ThoughT3 is more biologically active than its counterpart T4, secreted thyroid hormone is 90% T4. Peripherally much of T4 is converted to T3.

179
Q

Blood results in primary hyperthyroidism?

A
  • low TSH
  • raised T4 and T3
180
Q

Blood results of secondary hyperthyroidism?

A
  • e.g. pituitary adenoma
  • high TSH and raised T3 and T4
181
Q

Sublinical hyperthyroidism?

A

low TSH with a normal fT4 and fT3.

182
Q

autoab in graves?

A

Thyroid-stimulating hormone receptor antibodies (TSHR-Ab) are seen in > 90% of those with Graves’ disease.

183
Q

Imaging for hyperthyroidism?

A
  • Ultrasonography
  • Thyroid uptake scan
184
Q

Thyrotoxicosis

Thyroid uptake scan?

A
  • 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
Q

Initial therapy for hyperthyroidism?

A
  • 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
Q

symptomatic relief of hyperthyroidism?

A
  • A beta-blocker or calcium channel blocker may be prescribed to treat adrenergic symptoms whilst the thioamides take effect.
187
Q

radioactive iodine?

A

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
Q

CI for radioactive iodine?

A
  • Current pregnancy
  • Falling pregnantwithin 6 months of treatment
  • Breastfeeding
  • Fathering a childwithin 4-6 months of treatment
189
Q

cautions w radioactive iodine?

A
  • 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
Q

which ppts are offered radioactive iodine first line?

A
  • 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
Q

what may RAI aggrevate in graves?

A

can exacerbate or cause opthamology

192
Q

Propylthiouracil can be considered in adults where the patient is/has:

A
  • Intolerant/allergic to carbimazole
  • Pregnant or planning on pregnancy in the next 6 months
  • A history of pancreatitis
193
Q

What are the thionamides?

A
  • carbimazole
  • PTU
194
Q

Baselines before thionamides are started?

A
  • Baseline FBC and LFTs are obtained prior to the commencement of thioamides.
195
Q

what is a CI of thionamides?

A
  • Neutropenia or severely deranged transaminases are a contraindication to treatment.
196
Q

thyroidectomy?

A
  • 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
Q

complications of thyroidectomy?

A
  • hypocalcaemia
  • recurrent laryngeal nerve injury
198
Q

hypocalcaemia after thyroidectomy?

A
  • hypocalcaemia - typically transient, may be permanent in a minority of cases. Due to the proximity of the parathyroid glands to the thyroid gland.
199
Q

recurrent LN injury after thyroidectomy?

A
  • Recurrent laryngeal nerve injury: presents with hoarse voice post-operatively.
200
Q

thyrotoxic crisis may result from…

A
  • may result from decompensation during an illness
201
Q

how does thyrotoxic crisis present?

A
  • hyperthermia
  • tachycardia
  • arrhythmia
  • nausea
  • vomiting
  • seizures
  • cognitive decline
202
Q

Mx of thyrotoxic crisis?

A
  • BBs
  • thionamides
  • corticosteroids
  • Lugol’s iodine

tommy went to C a BTL

203
Q

Corticosteroids in thyrotoxic crisis?

A

reduced conversion of T4 to T3

204
Q

thyroid replacement therapy - prescription?

A
  • Advise the person to take LT4 medication on an empty stomach in the morning before other food or medication.
205
Q

Features of thyroid cancer?

A
  • Thyroid nodule/mass
  • Hoarseness/ change in voice
  • Cervical lymphadenopathy
  • Stridor
  • painless goitre
206
Q

Stridor =

A

harsh, high pitched sound, normally heard on inspiration, indicative of upper airway obstruction

207
Q

Features of thyroid malignancy on US?

A
  • Microcalcifications
  • Hypoechongenicity
  • Irregular margin
  • Increased vascularity
208
Q

Hypothyroidism - primary?

A
  • Primary hypothyroidism (overt):Elevated thyroid stimulating hormone (TSH) levels (typically > 10 mU/L) with a free T4 (fT4) level below the normal range.
209
Q

Subclinical hypothyroidism?

A
  • Subclinical hypothyroidism:The subclinical state is characterised by elevated TSH levels but T3/T4 that remains within the normal range
210
Q

secondary hypo?

A
  • 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
Q

tertiary hypo?

A
  • 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
Q

Resistance to thyroid hormone?

A
  • 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
Q

what happens in hashimotos?

A
  • ab mediated destruction of thyroid
214
Q

2 forms of hashimotos?

A
  • Goitrous:characterised by a firm and rubbery goitre
  • Atrophic:characterised by an atrophic gland
215
Q

epidemiology of hashimotos?

A
  • more freq seen in women
  • becomes inc common w age
216
Q

what is hashimotos assoc w ?

A
  • assoc w T1D, turners and downs syndrome
217
Q

what is the leading cause of hypothyroidism?

A
  • worldwide: iodine def
  • in the UK, hashimotos
218
Q

Amiodarone induced hypo - Wolff Chaikoff effect?

A
  • 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
Q

Amiodarone induced hypothyroidism - normal thyroid gland?

A

those with a normal gland may also develop hypothyroidism, frequently affecting T3.

220
Q

congenital hypothyroidism?

A
  • 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
Q

symptoms of hypo?

A
  • Tiredness
  • Lethargy
  • Weight gain
  • Cold intolerance
  • Reduced libido
  • Goitre
222
Q

menstrual changes in hypo?

A
  • Menstrual irregularities(oligomenorrhoea, amenorrhoea, menorrhagia)
  • everything gets heavy so periods get heavy
223
Q

signs of hypo?

A
  • Hair loss(characteristically the outer third of the eyebrows)
  • Dry skin
  • Goitre
  • Bradycardia
  • Myxoedema
  • Delayed relaxation phase of deep tendon reflexes
224
Q

Primary hypothyroidism =

A

raised TSH and reduced fT4.

225
Q

secondary/ tertiary hypo blood results =

A

normal (inappropriately normal) or lowered TSH or TRH and a reduced fT4.

226
Q

subclinical hypothyroidism?

A
  • Subclinical hypothyroidism refers to a raised TSH but normal fT4.
227
Q

Autoab in hashimotos?

A
  • Anti-TPO - hashimotos but can also be seen in graves
  • anti-Tg - hashimotos commonly
228
Q

TSHR-ab?

A
  • TSHR-ab - graves but can also be seen in hashimotos where they block TSh receptors preventing their activation
229
Q

other tests for hypo?

A
  • FBC
  • B12 and Folate
  • Serum lipids
  • HbA1c
  • Coeliac serology
230
Q

suspicion of malignancy ->

A
  • Ultrasonography
  • Specialist referral(urgent two week wait)
231
Q

Ix of hypothyroidism?

A
  • levothyroxine
  • TSH levels are checked every 2-3 months then yearly once stable
232
Q

myxodema coma often results from?

A
  • acute decompensation during an illness
233
Q

how do ppts w myexoedema coma present?

A
  • hypotension
  • hypothermia
  • bradycardia
  • cognitive decline
234
Q

Myxoedema coma Tx?

A

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
Q

Diagnosis of adrenal insufficiency involves?

A
  • random cortisol
  • 9am cortisol
  • short syncathen/ ACTH stimulation test
236
Q

9am cortisol?

A
  • 9am cortisol - cortisol levels highest in the morning
  • <100 nmol confirms adrenal insufficiency
237
Q

what is the definitive test for adrenal insufficiency?

A
  • Short synacthen /ACTH stimulation test (definitive test)
238
Q

short synacthen test?

A
  • normal resp is 30 min cortisol >550mmol/L
  • tests response to synthetic ACTH - how much cortisol is produced?
239
Q

primary vs secondary adrenal insufficiency?

A
  • primary adrenal insufficiency: defect within the adrenal gland
  • seconday adrenal insufficiency: defect in pituitary/ hypothalamus (ACTH/ CRH)
240
Q

acute management of P adrenal insufficiency?

A
  • Fluids: 1-3L of 0.9% Saline
  • Hypoglycaemia: iv dextrose
  • Glucocorticoids: Hydrocortisone
241
Q

LTM of P adrenal insufficiency?

A
  • hydrocortisone 3x day
  • fludocortisone once daily to replace aldosterone
  • ? androgen replacement
242
Q

sick day rules?

A

*Never stop steroids
*Double dose during illness/infection
*If unable to take PO Hydrocortisone, need IM/IV Hydrocortisone
*Carry steroid card / MedicAlert bracelet

243
Q

diagnosis of secondary AI?

A
  • deficiency of ACTH - no obv cause -> image pituitary
  • Failed SST
  • ACTH low or suppressed
  • History of exogenous steroid use
244
Q

CP of secondary adrenal insufficiency?

A
  • no hyperpigmentation - ACTH is low/ normal
  • no dehydration or hyperkalaemia - aldosterone intact
  • hypoglycaemia more common
  • clinical manifestations of tumour
245
Q

LTM of secondary adrenal insuffiency?

A
  • Hydrocortisone replacement
  • No need for Fludrocortisone
  • Taper steroids gradually
  • sick day rules
246
Q

management of secondary vs primary AI?

A
  • primary: hydrocortisone + fludorcortisone
  • secondary: just hydrocortisone no fludro
247
Q

what happens in addisons disease?

A

Primary adrenal insufficiency(Addison’s disease): caused by destruction or dysfunction of the adrenal cortex

248
Q

what happens in SAI?

A
  • 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
Q

TAI?

A

Tertiary adrenal insufficiency: caused by a reduction in corticotropin-releasing hormone, most commonly seen following chronic glucocorticoid steroid use.

250
Q

symptoms of AI - loss of glucocorticoid and mineralcorticoid function?

A
  • loss of normal glucocorticoid and mineralcorticoid function -> dehydration, weight loss, abd pain, nausea, vomiting, mood dist
251
Q

features of AI in women?

A
  • 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
Q

addisonian crisis?

A
  • addisonian crisis: medical emergency caused by profound glucocorticoid and mineralocorticoid deficiency that may be triggered by intercurrent illness.
253
Q

zones of the adrenal cortex?

A
  • zona glomerulasa
  • zona fasiculata
  • zona reticularis
254
Q

zona glomerulasa?

A

mineralocorticoids - aldosterone is the key mineralocorticoid, release primarily controlled by the renin-angiotensin system

255
Q

zona fasiculata?

A

glucocorticoids - release controlled by hypothalamic-pituitary-adrenal axis

256
Q

zona reticularis?

A

androgens - produces dehydroepiandrosterone (DHEA).

257
Q

adrenal medulla produces?

A
  • Adrenaline
  • Noradrenaline
  • Dopamine
258
Q

CRH is released from?

A

paraventricular nucleus of the hypothalamus.

259
Q

CRH ->

A
  • stimulates ACTH release from anterior pituitary
  • ATCH -> cortisol from adrenal cortex
  • cortisol exerts negative feedback on release of both ACTH and CRH
260
Q

Aldosterone?

A
  • released from zona glomerulasa of adrenal cortex
  • in response to: A2, ACTH, potassium levels
261
Q

aetiology of addisons - most common cause worldwide?

A
  • worldwide most common cause is TB
262
Q

most common cause of addisons in the west?

A

autoimmune adrenalitis

263
Q

other causes of addisons?

A
  • HIV
  • disseminated fungal infections
  • syphilis
  • malignant mets
  • amyloid deposits
  • bilateral adrenalectomy is iatrogenic
264
Q

how do ppts w addiosn tend to present?

A
  • 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
Q

features of addisons in women?

A
  • in women, androgen deficiency: loss of libido, loss of hair in axillary/ pubic regions
266
Q

what is spec to PAI?

A
  • hyperpigmentation - mucous membranes and palmar creases
267
Q

Signs of addisons

268
Q

When is it most commonly seen?

addisonian crisis is caused by?

A
  • 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
Q

addisonian crisis from addisons?

A
  • 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
Q

symptoms of addisonian crisis?

A
  • dehydration, hypotension and confusion, coma, pyrexia, shock, hyperpig
  • Blood tests may reveal hyponatraemia, hyperkalaemia and hypoglycaemia.
271
Q

addisons: aldosterone def ->

A

hyponatreamia and hyperkalamia

272
Q

Blood tests for AI?

A
  • morning cortisol < 100 - means AI very likely
  • 100-500 - AI possible
  • > 500 AI unlikely
273
Q

distinguishing between types of AI?

A
  • plasma ACTH
  • High: indicative of Addison’s disease (primary adrenal insufficiency)
  • Low: indicative of secondary/tertiary adrenal insufficiency
274
Q

short synacthen test?

A
  • 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
Q

Mx of addisons?

A
  • glucocorticoid replacement: hydrocortisone
  • mineralcorticoid replacement: fludocortisone
  • androgen replacement
276
Q

Mx of addisonian crisis?

A
  • IV hydrocortisone
  • IV fluid rehydration
277
Q

secondary AI?

A
  • inadequate ACTH -> adrenal glands not stim -> low cortisol
  • result of loss/ damage to pituitary gland
278
Q

What can lead to SAI?

A
  • Tumours(e.g., pituitary adenomas)
  • Surgeryto the pituitary
  • Radiotherapy
  • Sheehan’s syndrome
  • Trauma
279
Q

Sheehan’s syndrome?

A

where major post- partum haemorrhage causes avascular necrosis of the pituitary gland )

280
Q

TAI?

A
  • 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
Q

Pathophys of TAI?

A
  • When theexogenous steroids(originating outside the body) are suddenly withdrawn, thehypothalamusdoes not “wake up” fast enough, andendogenous steroids(originating inside the body) are not adequately produced.
  • Therefore, long-term steroids must be tapered slowly to allow theadrenal axisto regain normal function.
282
Q

symptoms of AI?

A
  • Fatigue
  • Muscle weakness
  • Muscle cramps
  • Dizziness and fainting
  • Thirst and craving salt
  • Weight loss
  • Abdominal pain
  • Depression
  • Reduced libido
283
Q

primary AI - skin?

A
  • Bronzehyperpigmentationof the skin, particularly in creases (ACTHstimulatesmelanocytesto producemelanin) - PRIMARY
284
Q

? ? is a sign of AI

A
  • Hypotension(particularlypostural hypotension– with a drop ofmore than 20 mmHgon standing)
285
Q

Autoantibodies may be present inautoimmuneadrenal insufficiency:

A
  • Adrenal cortex antibodies
  • 21-hydroxylase antibodies

Year 3 (45 decks)

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