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Endocrine Flashcards

1
Q

Describe the classical signs and symptoms of hyperthyroidism

A

Symptoms:

  • Anxiety/irritability
  • Heat intolerance/sweating
  • Increased appetite
  • Palpitations
  • Weight loss
  • Tremor
  • Loose motions
  • Fatigue/weakness

Signs:

  • Eyelid retration/lid lag
  • Graves’ opthalmopathy*
  • Goitre/bruit*
  • Systolic hypertension
  • Tachycardia/AF
  • Tremor
  • Hyper-reflexia
  • Warm peripheries
  • Acropachy*
  • Proximal weakness
  • Pre-tibal myxoedema*

*Signs specific to Grave’s disease

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2
Q

Describe the classical signs and symtoms of hypothyroidism

A

Symptoms:

  • Fatigue
  • Depression/psychosis
  • Cold intolerance
  • Weight gain
  • Constipation
  • Menorrhagia
  • Myxoedema coma (rare)

Signs:

  • Hair loss
  • Loss of outer third eyebrow
  • Anaemia
  • Hoarse voice
  • Goitre
  • Bradycardia
  • Dry skin
  • Hyporeflexia
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3
Q

List the common causes of hyperthyroidism

(outline pathophysiology of the most common)

A
  • Grave’s disease
    • IgG autoantibodies stimulate thyroid follicular cells, out of control of the normal pituitary feedback mechanism
  • Toxic multinodular goitre (toxic adenoma)
    • Commonly in older women, where several hyperactive nodules develop, outside of TSH control

Less common causes:

  • Solitary toxic adenoma (plummer’s disease) - same as toxic multinodular goitre but just one nodule
  • Thyroiditis
  • Drug-induced - Amiodarone, excess levothyroxine
  • Excess iodine intake
  • Hashitoxicosis - hyperthyroid phase of Hashimoto’s
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4
Q

List the common causes of hypothyroidism

(outline pathophysiology of the most common)

A
  • Hashimoto’s thyroiditis: assoicated with a goitre
    • Most common cause
    • T-cell destruction of the gland, plus B-cell secretion of inhibitory TSH-receptor antibodies
    • There is often an initial hyperthyroid phase
    • There is symmetrical, bosselated goitre
  • Previous treatment for hyperthyroidism
    • Thyroidectomy
    • Radioactive iodine

Less common causes:

  • Drugs: amiodarone, iodine excess, lithium
  • Iodine deficiency: most common cause worldwide
  • Thyroiditis: often transcient (not permanent)
  • Secondary causes:
    • Hypothalamic disorders
    • Pituitary disorders
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5
Q

What is goitre?

A

Goitre: painless enlargement of the thyroid gland

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6
Q

How can goitre be described?

A

There are certain characteristics to describe goitre:

  • Diffuse (spread all over) vs. nodular: pattern of swelling
  • Simple vs toxic: is it actively secreting thyroid hormone
  • Benign vs. malignant
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7
Q

What are the different types of nodular goitre?

Give the ddx for each one

A

Multinodular

  • Toxic multinodular goitre
  • Subacute thyroiditis

Solitary nodule

  • Follicular adenoma
  • Benign nodule
  • Thyroid malignancy
  • Lymphoma
  • Metastasis

Infiltration (rare)

  • TB
  • Sarcoid
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8
Q

How may the goitre cause physical problems?

A

With time, the goitre may extend to produce pressure symptoms on the trachea, oesophagus or veins. Extension may be retrosternal

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9
Q

What is the treatment for hyperthyroidism?

(primary and secondary care)

A

Primary care:

  • Non-selective ß-blocker, e.g. propanolol
    • 20-40 mg t.d.s. for rapid symptom relief
  • Refer to a specialist endocrinologist
    • If symptoms are not controlled on propranolol, consider starting carbimazole prior to specialist assessment

Secondary care:

  • Treatment options include antithyroid drugs, radioactive iodine therapy or surgical management
  • Patient’s with Grave’s disease are usually offered an intermediate course of antithyroid therapy, with the hope of inducing remission (50% success)
  • In other pathologies antithyroid drugs control but do not cure disease
    • Pts are offered radio-active iodine (RAI) or surgical managment (RAI 1st line)
    • Anti-thyroid drugs may be used long term if these therapies are unsuitable
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10
Q

Name two antithyroid drugs

(not an objective)

A

First line: Carbimazole

Second line: Propylthiouracil

Both act as a preferred substrate for thyroid peroxidase, the key enzyme in thyroid hormone synthesis

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11
Q

How is hypothyroidism treated?

A
  • Levo-thyroxine (L-T4) given (replacement therapy)
    • Low starting doses, titrated up to clinical effect
    • Reassess every 4-6 weeks, until TSH is in the lower half of reference range in primary disase
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12
Q

Describe HP thyroid axis

A
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13
Q

From a thyroid function test how can you tell if the abnormal functions are from disease of the thyroid or pituitary?

A
  • TSH levels will be high in pituitary disease (secondary hyperthyroidism); TSH levels will be low in disease originating from the thyroid gland itself (primary hyperthyroidism).
  • TSH levels will be low in secondary hypothyroidism (pituitary insufficiency); TSH levels will be high in primary hypothyroidism (thyroid insufficiency).
  • Misc: A raised TSH and T4 may reveal replacement therapy is inadequate, or thyroid hormone resistance is present (in pituitary gland)
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14
Q

How can you interpret thyroid autoantibody test results?

A
  • Antibodies for TPO and thyroglobulin are present in Hashimoto’s thyroiditis, and cause a decrease in hormone output. TSH blocking antibodies may also be present.
  • Antibodies for TSH receptors (IgG) are responsible for Graves’ disease; they stimulate the receptors and cause thyrotoxicosis. They may also be known as TSI. TPO and thyroglobulin antibodies may also be present.
  • Differentiation of TSI and TSH receptor blocking antibodies (TBII) may be undertaken by demonstrating inhibition of binding of TSH to its receptors, or by demonstrating stimulation of the release of cAMP.
  • TPO antibodies are found in 20% of the population, but only 10-20% of these people develop hypothyroidism.
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15
Q

How are malignant tumours in the thyroid gland classified?

A
  • Papillary carcinoma (most common 70%)
    • commonly presents 40-50
    • Risk factor: previous neck irradiation
    • Spreads locally, and metastasises to local nodes (can go to bone/lung but rare)
    • Prognosis good following either radio-iodine therapy or surgery
  • Follicular carcinoma (20% of tumours)
    • Metastasises via the bloodstream, classically bone
    • Same treatment and prognosis as papillary
  • Medullary carcinoma (5% of tumours)
    • Generally affects older adults
    • Can affect children/young adults as part of multiple endocrine neoplasia syndromes: MEN IIa/IIb
    • Arise from parafollicular/’C’ cells - so secrete calcitonin, so plasma calcitonin levels raised
    • Slow growing but poor prognosis
  • Anaplastic carcinoma (<5% of tumours)
    • Occurs in elderly populations
    • Extremely locally aggressive, with rapid and extensive local invasion (complications of tracheal and superior vena cava complications)
    • Poor prognosis
  • (Lymphoma is a differential for thyroid malignancy)
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16
Q

How do malignant tumours of the thyroid present?

A
  • Most present as asymptomatic thyroid nodules or lymph nodes
  • There may be hoarseness/dysphagia
  • Thyroid dysfunction is rare
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17
Q

How is a malignant tumour of the thyroid diagnosed?

A

Approach to solitary thyroid nodule:

  • History/examination
  • Ultrasound
  • Technetium scans:
    • ‘Hot’: suggests adenoma
    • ‘Cold’: may suggest malignancy
  • Fine needle aspiration and cytology
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18
Q

What hormones are released by the adenohypophysis? (anterior pituitary)

A
  • Growth hormone
  • Prolactin
  • Adrenocorticotropic hormone (ACTH)
  • Thyroid stimulating hormone (TSH)
  • Gonadatrophin luteinizing hormone (LH)
  • Follicle stimulating hormone (FSH)
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19
Q

What hormones are released by the neurohypophysis? (posterior pituitary)

A
  • Anti-diuretic hormone (ADH)
  • Oxytocin
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20
Q

Classify pituitary adenomas according to size and function

A

Prolactinoma (40- 50%)

  • SIZE: In younger women, most 10mm. In men and elderly women, many >10mm
  • Hormonal signs and symptoms:
    • Galactorrhoea
    • Amenorrhoea
    • Hypogonadism
    • Erectile Dysfunction

GH secreting tumour (20%)​

  • SIZE: Mm to Cm
  • Hormonal signs and symptoms:
    • Change in appearance, increase in height.
    • Acromegaly/Gigantism

ATCH secreting tumour (10-15%)

  • SIZE: Majority <10mm
  • Hormonal signs and symptoms:
    • Cushing’s disease

TSH secreting tumour (rare)​

  • SIZE: Most >10mm
  • Hormonal signs and symptoms:
    • Hyperthyroidism

Non-functioning (20%)

  • SIZE: ​Most >10mm at presentation
  • Hormonal signs and symptoms:
    • Hypopituitarism
    • Mechanical S/s.
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21
Q

What is a pituitary adenoma?

How are they classified?

A
  • Benign tumours of the glandular tissue in the pituartary
    • Can be life threatening due to mass effects or secretory action
  • Tumours <1cm are classified as microadenomas
  • Tumours >1cm are classified as macroadenomas
  • Classidied as ‘functioning’ or ‘non-functioning’ (silent) on the basis of whether they are secretory or nor
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22
Q

What are the local symptoms that result from a large pituitary adenoma?

(the non-functioning adenoma presentation)

A

Local symptoms are caused by impingement or pressure upon surrounding structures

  • Bitemporal hemianopia: compression of the optic chiasm
  • Ocular palsies: compression of cranial nerves III, IV & VI
  • Hypopituitarism: destroys the normal functioning tissue
  • Signs of raised ICP: headache
  • Hypothalamic compression symptoms: altered appetite, thirst, sleep/wake cycle
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23
Q

What are the systemic clinical consequences of pituitary adenoma?

(functioning adenoma presentation)

A

Think about what hormones are released by the pituitary

  • Acromegaly: excessive GH production
  • Hyperprolactinaemia: excessive prolactin production
  • Cushing’s syndrome: excessive ACTH production

Tumours secreting LH, FSH and TSH are rare.

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24
Q

What is Cushing’s syndrome?

What are its causes?

A

Cushing’s syndrome describes the symptoms of increased circulating glucocorticoid

  • ACTH dependent causes:
    • Cushing’s disease
      • Increased ACTH from anterior pituitary (65%)
    • Ectopic ACTH
      • Non-pituitary ACTH secreting tumour (10%) (classically small-cell lung cancer)
  • ACTH independent causes:
    • Excess adrenal cortisol production
      • Due to an adrenal tumour or nodular hyperplasia: 25%
      • Subsequent physiological ACTH suppression
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25
Q

What are the major clinical and biochemical features of Cushing’s syndrome?

(signs and symptoms)

A

Symptoms:

  • Central weight gain
  • Change in appearance
  • Depression
  • Insomnia
  • Poor libido
  • Thin skin/easy bruising
  • Excess hair growth/acne
  • Diabetes symptoms

Signs:

  • Moon face
  • Frontal balding
  • Striae
  • Hypertension
  • Pathological fractures
  • ‘Buffalo hump’ (dorsal fat pad on back of neck)
  • Proximal myopathy
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26
Q

What is Addison’s disease?

What are its causes?

A
  • Primary adrenal insufficiency
  • Destruction of the entire adrenal cortex leading to glucocorticoid (cortisol), mineralocorticoid (aldosterone), and sex-steroid deficiencies
  • This differs from hypothalamic-pituitary (HPA) disease as HPA disease generally spares mineralocorticoid production, which is stimulated by ATII (sex steroids are also largely independent of pituitary stimulation)

Causes:

  • Autoimmune: 80% in the UK
  • TB: most common cause worldwide
  • Overwhelming sepsis
  • Metastatic cancer: lung/breast
  • Lymphoma
  • Adrena haemorrhage
    • Waterhouse-Friderichsen syndrome
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27
Q

What are the signs and symtoms for addison’s disease?

A

Symptoms: (often vague and non-specific)

  • Weight loss
  • Malaise
  • Weakness
  • Myalgia (muscle pain)

Signs:

  • Pigmentation, especially of new cars and palmar creases
  • Postural hypotension
  • Signs of dehydration
  • Loss of body hair (paticularly axillary/pubic)
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28
Q

What is Conn’s syndrome?

A
  • Adrenal adenoma leading to primary hyperaldosteronism (excess production of aldosteronism from adrenal glands)
    • (Conn’s syndrome is responsible for primary hyperaldosteronism in 60% of cases)
  • Hyperaldosteronism leads to sodium and water retention
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29
Q

How does Conn’s syndrome present?

What are its biochemical features?

A

Presentation:

  • Mostly asymptomatic
  • Hypertension
    • resistant to treatment
    • may causes headaches
  • Features of hypokalaemia
    • May cause cramps, weakness, tetany
    • May be polyuria

Biochemical features:

  • Hypokalaemia, with urinary potassium loss
  • Elevated plasma aldosterone:renin ratio
    • Plasma aldosterone levels will not be suppressed by fludrocortisone administration
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30
Q

What is phaeochromocytoma?

A

A neuroendocrine tumor of the medulla of the adrenal glands (originating in the chromaffin cells), or extra-adrenal chromaffin tissue that failed to involute after birth,that secretes high amounts of catecholamines, mostly norepinephrine, plus epinephrine to a lesser extent

31
Q

How many parathyroid glands are there and where are they?

When is parathyroid hormone secreted?

What does it do?

A
  • There are 4 parathyroid glands, lying posteriorly to the thyroid
  • The chief cells are responsible for secreting parathyroid hormone (PTH)
    • PTH is secreted when plasma calcium levels are low
    • PTH can also be secreted in response to low vitamin D, or high phosphate levels
  • PTH works to increase plasma calcium reabsorption from bone by:
    • Directly stimulating calcium resabsorption from bone
    • Directly increasing renal tubular calcium reabsorption
    • Indirectly stimulating increased GI calcium absorption
      • By increasing vitamin D activation in the kidney
    • PTH has a secondary effect of increasing renal phosphate excretion
32
Q

What is the role of vitamin D?

How is ‘active’ vitamin D formed?

A

Vitamin D acts to sustain plasma calcium and phosphate levels by increasing their inflow from the GI tract

  • It i also required for normal bone formation
  • Endogenously it is synthesized in the skin, forming D3, cholecalciferol
  • Exogenously it is ingested as D2, ergocalciferol (common in fish, liver and dairy products)
  • ‘Active’ vitamin D is then formed by a second hydroxylation in the kidney, to produce to 1,25-(OH)2-D2/3
33
Q

What are causes of vitamin D deficiency?

A

Most commonly occur in people with inadequate sunlight exposure, malabsorptive conditions and liver/kidney disease

34
Q

Where is calitonin secreted from?

What is its function?

A
  • Calcitonin is secreted by parafollicular/’C’ cells of the thyroid gland in response to increased plasma calcium levels
  • It acts to decrease plasma calcium levels, by antagonism of the effect of PTH on the bone
35
Q

Why is the importance of calcitonin in humans is controversial?

A
  • Removal of thyroid, and complete calcitonin deficiency does not lead to overt hypercalcemia
  • Extreme hypersecretion of calcitonin by tumours rarely produces hypocalcaemia
  • It is likely that PTH/Vitamin D levels are adjusted in response to calcitonin changes
36
Q

Give an overview of the normal control of serum calcium

A
  • Intestinal uptake of calcium depends on the amount of ionized calcium in the lumen, and the presence of activated vitamin D
  • 90% of renal excretion of calcium is related to sodium reabsorption in the proximal tubule, with 10% regulated by PTH in the distal tubule
37
Q

What are the common causes of raised serum calcium?

A

In a patient with hypercalcaemia, 97% of cases are due to primary hyperparathyroidism or malignacy (PTH high in hyperparathyroidism, low in malignancy)

Causes:

  • Excessive PTH secretion
    • Primary hyperparathyroidism
    • Tertiary hyperparathyroidism
    • Ectopic PTH secretion (very rare)
  • Malignancy
    • Myeloma
    • Metastatic deposits in bone
    • Paraneoplastic
      • PTHrp secretion: e.g. SCC (of lung or other tissues)
      • Production of osteoclastic factors
  • Excess Vitamin D
    • Exogenous excess
    • Granulomatous disease: TB/sarcoid
    • Lymphoma
  • Excess calcium intake
    • ‘Milk-alkali’ syndrome (antacids + large amounts of calcium lead to excessive absorption
  • Other endocrine disease
    • Thyrotoxicosis
    • Addison’s
  • Renal disease
    • Severe AKI
  • Drugs
    • Thiazide diuretics
    • Lithium
  • Hereditary
    • Familial hypocalciuric hypercalcaemia
38
Q

What are the symptoms of hypocalcaemia?

A
  • Peripheral irritability:
    • Tetany/cramps
    • Carpo-pedal spasm
      • Wrist flexion and fingers drawn together
      • Happens especially after occulusion of brachial artery, e.g. with a blood pressure cuff: Trosseau’s sign
      • Tapping over the facial nerve causes twitches: Chvostek’s sign
  • Central irritability
    • Seizures
  • Depression/anxiety
  • Perioral paraesthesia
  • Cataracts
39
Q

What the common causes of hypocalaemia?

A

With low PTH (hypoparathyroidism)

  • Idiopathic/primary hypoparathyroidism (autoimmune)
  • Post thyroid/parathyroid surgery
  • Post neck irradiation
  • Infiltration: sarcoid/malignancy
  • Congential absence of the gland: Digeorge syndrome
  • Severe hypomagnesia: impairs PTH secretion

With high PTH

  • Vitamin D deficiency
  • Acute pancreatitis
  • Alkalosis
  • Acute hyperphosphataemia
    • renal failure
    • rhabdomyolysis
    • tumour lysis
  • Drugs: bisphosphonates, calcitonin
40
Q

Describe the WHO classification of:

  1. Diabetes mellitus
  2. Impaired glucose tolerance
  3. Impaired fasting glycaemia
A
  1. Diabetes mellitus - a metabolic disorder of multiple causes characterized by chronic hyperglycaemia resulting from defects in insulin secretion, insulin action or both
  2. Impaired glucose tolerance (IGT) is a pre-diabetic state of hyperglycemia that is associated with insulin resistance and increased risk of cardiovascular pathology.
  3. Impaired Fasting Glycaemia is a type of prediabetes, in which the blood sugar level during fasting is consistently higher than what are considered normal levels; however, the level is not high enough to be diagnosed as diabetes mellitus. This pre-diabetic state is associated with insulin resistance and increased risk of cardiovascular pathology, although of lesser risk than impaired glucose tolerance (IGT). Patients identified to have IFG should undergo the 2hr glucose test to rule out IGT.
41
Q

What are the blood gluose values for normal, diabetes, impaired glucose intolerance and impaired fasting glucose?

A

Normal

  • Fasting: <6.1
  • 2hr after 75g glucose: <7.8

Impaired fasting glycaemia

  • Fasting: >6.1
  • 2hr after 75g glucose: n/a

Impaired glucose tolerance

  • Fasting: 6.1-7.0
  • 2hr after 75g glucose: 7.8-11.1

Diabetes Mellitus

  • Fasting: >7.0
  • 2hr after 75g glucose: 11.1
42
Q

Classify the major types of diabetes mellitus

A

Type I DM:

  • Autoimmune disease, with autoantibodies targeted against the insulin-secreting ß cells of the Islets of Langerhans in the pancreas, leading to cell death and inadequate insulin secretion
  • It is hypothesised that viral infection

Type II DM:

  • Unlike type I diabetes, blood insulin levels are initially normal, or even increased in the early stages to compensate for insensitivity of the bodily tissues to the insulin
  • The ‘insulin resistance’ is associated with aging, genetic factors, obesity, high fat diets and a sedentary lifestyle
  • Eventually the ß cells decompensate, and can no longer produce excess insulin, leading to hyperglycaemia

Gestational Diabetes Mellitus

  • may occur during pregnancy. It results in a similar hyperglycaemia, of variable severity, recognised first during pregnancy. Impaired glucose control may antedate pregnancy.
  • Capillary glucose levels for impaired glucose tolerance are used for diagnosis with clinical symptoms.

Maturity Onset Diabetes of the Young (MODY)

  • may represent 5-10% of diabetic patients.
  • This form of diabetes is clinically similar to T2DM but presents in young patients
43
Q

What are the secondary causes for 1% cases of diabetes?

A
  • Pancreatic disease:
    • CF, chronic pancreatitis, pancreatic carcinoma
  • Endocrine disease:
    • Cushing’s disease, acromegaly, thyrotoxicosis, PCC, glucagonoma
  • Drug induced:
    • Thiazide diuretics, corticosteroids, antipsychotics, antiretrovirals
  • Congential disease:
    • Insulin receptor abnormalities, myotonic dystrophy, Friedreich’s ataxia
44
Q

What are the typical presentations of a patient with Type I DM?

A
  • Presents in childhood/aldolescence with a 2-6 week history of;
    • Polyuria: high sugar content in urine leading to osmotic diuresis
    • Polydipsia: due to resulting fluid loss
    • Weight loss: fluid depletion plus fat/muscle breakdown
  • Diabetic Ketoacidosis (DKA) is also a common first presentation
45
Q

What are the typical presentations of a patient with Type II DM?

(compare and contrast with type I DM)

A
  • The clinical onset may be over many months/years, with the classic triad of symptoms present, but less obvious than in type I DM
  • More common presenting features are:
    • Lack of energy
    • Visual blurring: glucose-induced refractive changes
    • Pruritis vulvae/balantitis: due to candida infection
  • In older patients, it may be the complications of diabetes that are the presenting feature:
    • Retinopathy: noted by the optician
    • Polyneuropathy: tingling and numbness in the feet
    • Erectile dysfunction
    • Arterial disease: MI/peripheral vascular disease
  • Type II DM is recognised as part of the metalbolic syndrome:
    • T2DM
    • Central obesity
    • Dyslipidaemia: low HDL cholesterol, hypertriglyceridaemia
46
Q

List the clinical features of type I diabetes mellitus

A
  • Ketoacidosis
  • younger patient
  • polyuria
  • polydipsia
  • weight loss
  • onset over weeks.
47
Q

What are the priciples of the dietary treatment of type 1 and type 2 diabetes?

A

Diet: no different to that considered healthy for everyone:

  • High in low-GI carbohydrates
  • Limit foods high in sugar and saturated fats
  • Diabetic specific foods are not required
  • Can see nutritionist to help with meal plans
  • Allowed alchol but may exacerbate/prolong effect of hypoglycaemic drugs and may make the signs of hypo less clear

Toms guide:

Protein – 1g/kg Fat - <35% total intake. Keep sat+trans fat<10% of total intake. CHO – 40-60% of total intake. Choose low GI foods. Fruit, vegetables, some alcohol allowed. Salt < 6g Recommend fibre. Salt <6g a day (<3g a day in hypertensive diabetic patients)

48
Q

Describe the methods of evaluating diabetic control

A

Urine testing;​

  • Urine tests using dipsticks give patients who do not use blood testing some idea of how well controlled their glucose levels are. However, the relationship between urine glucose levels and blood glucose levels is not exact, for 3 main reasons:
  1. changes in urine glucose lag behind blood changes
  2. the mean renal threshold is 10mM, but the range is wide
  3. urine tests can give no guidance concerning glucose levels below the renal threshold (hypos go unchecked)

Home blood glucose testing

  • Home blood glucose testing is the best place for assessment of day-to-day control, and is an essential aid to that control.
  • Patients are able to control their insulin dose appropriately.
  • Patients should generate a profile, for example: 4 tests aday, 2 days a week; and share this with nurses to help enable the best system available for them to be used.

HbA1c:

  • HbA1c is generated as a two step reaction eventually resulting in glucose attaching to the valine in the Beta chain of a Hb molecule.
  • The rate at which this occurs depends on glucose concentrations. Normal range is between 4-6.2% (<48). This gives us an idea of control of blood glucose levels over the lifespan of Hb, about 6 weeks.
  • Should be checked 6 monthly
  • The figure will be misleading in anaemia, thalassaemia, haemoglobinopathy or pregnancy, in which case the shorter-term fructosamine test may be used.
49
Q

What are the two major hyperglycaemic complications of diabetes?

A

Diabetic Ketoacidosis

  • metabolic emergency in which hyperglycaemia is associated with metabolic acidosis due to greatly raised ketone levels
  • It is associated with type I DM but can rarely occur in type 2 DM

Hyperosmolar Hyperglycaemic State

  • Characteristic of type 2 DM, a severe hyperglycaemia causes a hyperosmolar state in absence of severe ketosis
50
Q

Outine the metabolic pathway that underlie diabetic ketoacidosis (DKA)

(pathogenesis)

A
  • Absolute insulin deficiency leads to uncontrolled catabolism
  • In the absence of insulin, hepatic glucose production is increased, and peripheral uptake of glucose is reduced
  • Rising glucose levels leads to an osmotic diuresis, leading to severe dehyrdation
  • Rapid lipolysis occurs in glucose-starved tissues, leading to elevated free fatty acids, which are converted to fatty acetyl-CoA in liver cells
  • Fatty acetyl-CoA can be converted to ketone bodies in mitochondria to generate energy
  • Accumulation of ketone bodies causes a metabolic acidosis (can be detected on breath)
  • Respiratory compensation leads to hyperventilation
  • Acidosis causes vomiting, and further fluid/electrolyte loss
  • Renal perfusion falls, leading to impaired excretion of the raised H+ and ketones
    • There is increased excretion of sodium and potassium
    • Despite a significant total body deficit of K+, initial serum K+ is typically normal, or even elevated (pseudo-hyperkalaemia)
    • This is due to extracellular migration of K+ in response to acidosis & insulin deprivation
    • Serum K+ levels will then usually fall during treatment as the exogenous insulin drive K+ into cells
    • If serum K+ is not monitored and replaced as needed, life-threatening hypokalaemia may develop
51
Q

What are common resons for the development of DKA?

A
  • Previously undiagnosed diabetes
  • Interruption of insulin therapy
  • The stress of intercurrent illness/surgery
52
Q

What is hyperglycaemic hyperosmolar syndrome (HHS)?

Who does it occur in?

What are precipitating factors?

A
  • Severe hyperglycaemia causes a hyperosmolar state in the absence of severe ketosis
  • Typically occurs in the elderly, often with undiagnosed T2DM
  • Precipitating factors:
    • Consumption of glucose-rich fluids
    • Medications: thiazide diuretics, steroids, B-blockers
    • Intercurrent illness: infection/MI
  • These patients may be more severely dehyrdated than DKA patients, but there will be no raised ketones (can be lactic acidosis but is generally mild)
53
Q

What are the clinical presentations of DKA?

A
  • Prostration (collapse - complete physical or mental exhaustion)
  • Kussmaul respiaration: air hunger
  • Nausea & vomiting
  • Abdominal pain
  • Confusion/stupor

On examination there may be evidence of marked dehydration, with the smell of ketones of breath. There is often a history of marked polyuria (litres)

54
Q

What are the clinical features of Hyperosmolar hyperglycaemic state (HSS)?

A
  • Dehydration
  • Stupor/coma/seizures
  • Evidence of an underlying illness
55
Q

Describe the clinical symptoms of hypoglycaemia.

How are they grouped?

A

Hypoglycaemia is defined as plasma glucose <3mmol/L, but individual thresholds for symptoms are variable. Symptoms are autonomic or neuroglycopenic:

Autonomic:

  • Sweating
  • Anxiety
  • Hunger
  • Tremor
  • Palpitations

Neuroglycopenic:

  • Confusion
  • Drowsiness/coma
  • Seizures
56
Q

What are the major counter-regulatory hormone responses to hypoglycaemia?

What does it do?

A

In episodes of hypoglycaemia, the aplha cells of the pancreas will release glucagon, which works to:

  • Increase glycogenolysis
  • Increase gluconeogenesis
  • Inhibit glycogen synthesis

The adrenaline response may be absent in patients with a long history of diabetes (associated with a loss of warning symptoms).

Growth hormone and cortisol may be released over a longer period of time to give a small increase in blood glucose levels

57
Q

Why might a patient develop hypoglycaemia?

A

In type I DM, the alpha cells (of pancreas) become insensitive to falls in glucose, thus becoming increasingly vulnerable to hypoglycaemia

Aetiology of hypoglycaemia:

  • Excess insulin
    • Inhibits hepatic gluconeogenesis and glycogenolysis
    • Either exogenous or insulinoma
  • Depletion of hepatic glycogen
    • Malnutrition, fasting, exercise or alcohol
    • Liver failure can also cause this

Pituitary insufficiency, adrenal insufficiency and non-pancreatic neoplasms can also cause hypoglycaemia

58
Q

What is the treatment of hypoglycaemia?

if able to swallow

A
  • Prompt consume 10-20g of fast-acting form of carbohydrate, preferably in liquid form (lucozade)
  • Recheck blood glucose levels after 10-15 minutes
    • Hypoglycaemia should be reversed in about 10 minutes
    • Improvements in signs and symptoms may lag behind improvement in blood glucose
  • If inadequate response, repeat as above and recheck again
  • When symptoms improve, the patient should eat some long-acting carbohydrate
59
Q

What is the treatment of hypoglycaemia?

if unconscious/ unable to swallow (severe hypoglycaemia)

A
  • Administer IM glucagon immediately
    • If <8 years old: 500 micrograms
    • If >8 years old: 1mg
  • If glucagon not available, the patient has consumed alcohol (glucagon not effective if alcholol drunk), or the person does not respond to glucagon within 10 minutes, call 999 for emergency hospital transfer - IV treatment
  • If the patient responds to glucagon, advise intake of long-acting carbohydrates when able
  • Vomiting is common during recovery, which can precipitate further episodes of hypoglycaemia
  • Within hospital, 100ml of 20% glucose can be used as an alternative to glucagon, and this can be repeated 3 times

Following recovery, never omit insulin in patients with T1DM

60
Q

Interpret blood gases showing a metabolic acidosis due to DKA

A

Metabolic acidosis will show a low pH, negative base excess and compensatory low pCO2.

61
Q

What are the microvascular complications of diabetes?

A

Microvascular disease, unlike macrovascular disease is specific to diabetes.

  • Small vessels of the retina, glomeruli and nere sheaths are particuarly affected
  • Symptoms manifest 10-20 years after diagnosis in young patients

Diabetic eye disease - Most common cause of blindness in under 65s

Diabetic Retinopathy (DR) - can be non-prolifertive (NPDR) or proliferative (PDR)

Diabetic malculopathy - retinopathy that affects the macula

Cataract formation - clouding of the lens in the eye which leads to a decrease in vision

Glaucoma - optic nerve damaged

62
Q

Describe what diabetic retinopathy is in more detail?

Types?

A

It can be non-proliferative (NPDR) or proliferative (PDR)

Non-proliferative diabetic retinopathy (NPDR)

  • ​Usually asymptomatic, and always occurs at some severity after 8-10y of DM
  • Features on fundoscopy;
    • Micro-aneurysms
    • Exudates: due to leaky vasculature
    • Haemorrhages: dot, blot, flame shaped
    • Cotton wool spots (>5 indicates ‘pre-proliferative’ retinopathy)
  • Can progress into proliferative diabetic retinopathy

Proliferative diabetic retinopathy (PDR) -more common in T2DM

  • Characterised by the development of new vessels on the optic disc or retina as a response to significant retinal ischaemia (ischaemia leads to vascular endothelial growth factor (VEFG) production)
  • The vessels are fragile, and likely to bleed with the traction that occurs when they are growing forward to give a pre-retinal or vitreous haemorrhage
  • If untreated, the blood vessels will cause fibrosis and a tractional retinal detachment, again leading to loss of acuity
  • They can also cause acute angle closure glaucoma due to iris neovascularisation, known as rubeosis iridis
63
Q

Describe diabetic maculopathy is more detail

How does it present?

Types?

A
  • More common in type II diabetes
  • Maculopathy is damage to the macula, the part of the eye which provides us with our central vision. A common from of damage is from diabetic macular oedema (DMO) in which fluid builds up on the macula.
  • Typically presents with as blurring of vision
  • 3 subtypes: focal, diffuse and ischemic
64
Q

What is cataracts?

Symptoms?

Is it more likely in diabetics?

A

A cataract is a clouding of the lens in the eye which leads to a decrease in vision

  • Symptoms are trouble with bright light/headlights and reading vision
  • Increased rates of age-related cataracts in diabetics
    • Postior sub-capsular cataracts are the most common
65
Q

List the neurological complications of diabetes mellitus

A
  • Symmetrical polyneuropathy
  • Acute painful neuropathy
  • Mononeuropathy
  • Diabetic amyotrophy
  • Autonomic neuropathy
66
Q

What is symmetrical polyneuropathy?

A
  • ‘Glove and stocking’ sensory loss, with vibration, deep pain and temperature lost first
  • Patients complain of losing their balance when eye are closed, e.g. when washing their face, due to proprioception (walking on cotton walk feeling is common)
  • Interosseous wasting of the small muscle of the feet results in a charactistic foot shape, and abnormal pressure areas lead to ulcers
  • Unrecognised trauma with poor wound healing may also lead to ulcers
  • Neuropathic arthropathy can also develop -Charcot’s foot - progressive degeneration of a weight bearing joint, a process marked by bony destruction, bone resorption, and eventual deformity
67
Q

What is acute painful neuropathy?

A
  • Painful burning pains in the feet, shins and anterior thighs
  • Associated with poor glycaemic control
  • Typically worse at night (pressure from bedclothes may be intolerable)
  • Usually remits after 3-12 months of good glycaemic control
  • More chronic forms may be resistant to all forms of therapy
68
Q

What is mononeuropathy?

What types of mononeuropathy may occur in diabetes?

What is mononeurtis complex?

A
  • Type of damage to nerves outside the brain and spinal cord

Commonest types of mononeuropathy that may occur in diabetes:

  • Cranial nerve lesions can occur in patients with diabetes
    • Mainly CNs III, IV and VI; ocular palsies
  • Isolated peripheral nerve lesions can also occur
    • Any nerve compression syndrome is more common in diabetes, e.g. carpal tunnel syndrome
    • Foot drop may occur due to lesions of the sciatic nerve
  • When more than one nerve is affected, this is known as mononeuritis complex
69
Q

What is diabetic amyotrophy?

How does it present?

A
  • Amyotrophy is progressive wasting of muscle tissues
  • It is rare, usually developing in middle aged men
  • In diabetes, it presents as painful wasting of quadriceps
  • Course is variable, often with gradual but incomplete improvement
70
Q

What is autonomic neuropathy?

How does it present?

A
  • Autonomic neuropathy is a group of symptoms that occur when there is damage to the nerves that manage every day body functions
  • Sympathetic dysfunction leads to postural hypotension, ejaculatory failure, reduced sweating and Horner’s syndrome
  • Parasympathic dysfunction leads to erectile dysfunction, constipation, urinary retention and a Holmes-Adie pupil (large and irregular pupil)
71
Q

Outline the natural history of renal complications of diabetes

A
  • Usually manifests 15-25 years after diagnosis
  • CKD is leading cause of premature death in young diabetics (neuropathy will affect 30%)
  • Most important intervention is adequate blood pressure control
72
Q

What are the macrovascular complications of diabetes?

A
  • Diabetes is a risk factor in the development of atherosclerosis
  • Increased risk:
    • 2x increased risk of stroke
    • 4x increased risk of MI
    • 50x increased risk of amputation for gangrene
73
Q

What are the causes and consequence of diabetic foot?

A
  • 10-15% of diabetic patients develop foot ulcers at some point in their lives.
  • Foot problems are responsible for 50% of diabetes-related hospital admissions.
  • Ischaemia, infection and neuropathy combine to produce tissue necrosis.
  • Medical supervision and patient education hope to reduce the number of amputations required.
  • Patients may lose some proprioceptive function and fall more easily.

CP1 (13 decks)

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