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BPT > Summary Book Endocrine > Flashcards

Summary Book Endocrine Flashcards

1
Q

Examination steps for hyperthyroidism

A

Thyroid followed by cardio, then upper limb reflex and confirm proximal myopathy

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2
Q

What are increased beat adrenergic effects

A

hyperreflexia, bounding pulse, tremor, sweaty palm, tachycardia, atrial fibrillation, flow murmur, high output heart failure

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3
Q

Graves eye signs

A

proptosis, exophthalmos, ophthalmoplegia

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4
Q

Diffuse goitre with bruit

A

graves or if hypothyroid then iron deficiency or chronic autoimmune

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5
Q

Nodular goitre ddx

A

MNG, nodule, cancer

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6
Q

Tender goitre

A

thyroiditis

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7
Q

Retrosternal goitre examination findings

A

pembertons sign and dullness to percussion

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8
Q

Cause of hoarseness

A

Recurrent laryngeal nerve palsy

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9
Q

Signs of hyperthyroidism

A

If graves = proptosis, exophthalmos, ophthalmoplegia. Goitre. Increased cardiac rate wit possible associated failure. Proximal myopathy, hyperreflexia, tremor, sweaty, hypopigmentation of skin, nail changes (thyroid acropachy = clubbing, swelling, periosteal reaction), accelerated bone remodelling with risk of osteoporosis, pretibial myxoedema

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10
Q

Autoimmune conditions associated with hyperthyroidism

A

diabetes mellitus, vitiligo, coeliac disease

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11
Q

Aetiology for hyperthyroidism

A

Autoimmune = graves and Hashimoto. Drug induced = amiodarone (type 1 increases synthesis due to iodine load, type 2 due to thyroid toxicity). Multinodular goitre, toxic nodule, thyroiditis (infectious, ischaemic, lymphocytic), hCG mediated, TSH dependant (TSHoma), iodine induced, paraneoplastic, iatrogenic (thyroxine therapy), factitious

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12
Q

Investigations for hyperthyroidism

A

Thyroid function tests (TSH secreted by anterior pituitary), T3/4, thyroid antibodies, TSH receptor (graves = activating, Hashimoto = inhibiting), thyroid peroxidase (hashimoto thyroiditis - most common), thyroglobulin. Can also consider ultrasound, radioactive iodine uptake and biopsy.

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13
Q

Management of graves disease.

A

Symptom control - beta blocker. Reduced thyroid hormone synthesis - thioamides (carbimazole or propylthiouracil), radioactive iodine ablation, thyroidectomy. Adjunctive therapies - corticosteroids (inhibit peripheral conversion and secretion). Management of orbitopathy - smoking cessation, if severe radioactive iodine is contraindicated, corticosteroids, Teprotumumab, Tocilizumab, Rituximab.

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14
Q

Examination for hypothyroidism

A

Thyroid plus hand, then upper limb reflex

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15
Q

Signs of decreased beta adrenergic effects

A

slowed mentation, hyporeflexia, bradycardia, pericardial effusion, obesity

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16
Q

Signs of hypothyroidism

A

goitre, hyporeflexia, slowed mentation, bilateral ptosis, loss of distal eyebrows, tongue swelling, macroglossia, bradycardia, pericardial effusion, proximal myopathy, carpel tunnel syndrome, dry skin and hair thinning, weight gain, ascites, other autoimmune conditions

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17
Q

Aetiology of hypothyroidism

A

Autoimmune - hashimoto. Thyroid organ failure - atrophy, infiltration, ischaemic, fibrosis, post infectious, amiodarone. Thyroiditis. Iatrogenic - radioactive iodine, thyroidectomy. TSH dependent - pituitary or hypothalamic. Thyroid hormone resistance.

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18
Q

TFT finding differences between primary, secondary and tertiary hypothyroidism

A

Primary = TSH >10, low T3/4. Secondary = low TSH, low T3/4. Tertiary = low TSH, low T34, low thyroid releasing hormone.

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19
Q

Goals and strategy for management of hypothyroidism

A

Goals = symptom management, normalise TSH, avoid iatrogenic hyperthyroidism. To normalise TSH titrate levothyroxine (T4).

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20
Q

When should levothyroxine be increased or decreased?

A

Increase in pregnancy. Decrease in weight loss, aging and androgen therapy.

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21
Q

Examination for cushings syndrome

A

Skin with blood pressure and proximal myopathy

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22
Q

Pathophysiology of cushings syndrome

A

high cortisol

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23
Q

Signs of cushings syndrome

A

cognitive dysfunction / psychosis, increased facial width, dorsal fat pad, skin pigmentation, hypertension, decreased limb fat, thin skin / bruising, osteoporosis, insulin resistance, increased abdominal fat, abdominal striae, hypogonadism, hypercoagulable state and increased infection risk

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24
Q

Organ and ddx of primary cushings syndrome

A

Adrenal. DDX: adenoma, carcinoma, bilateral macronodular adrenal hyperplasia, primary pigmented nodular adrenocortical disease.

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25
Q

Organ and ddx of secondary cushings syndrome

A

Anterior Pituitary = Cushings Disease. DDX: ACTH -secreting pituitary adenoma.

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26
Q

Organ and ddx of tertiary cushings

A

Hypothalamic. DDX: CRH secreting lesion.

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27
Q

Most common and oncological causes of cushings

A

Most common is endogenous with steroid use. Paraneoplastic causes of cushings are SCLC, pancreatic and thyroid.

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28
Q

Investigations for suspected cushings

A
  1. Exclude steroids. 2. Demonstrate hypercortisolism with either 24hr urinary cortisol, midnight salivary cortisol or low dose dexamethasone suppression test. 3. Also serum ACTH (<1.1 = ACTH independence, >4.4 ACTH/CRH dependence). 4. If low ACTH can use high dose dexamethasone suppression test = if cortisol <5 microg/dL then pituitary cause, if no suppression then ectopic. 5. CRH stimulation test -> ACTH response = pituitary, no response = ectopic.
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29
Q

Tests for suspected primary cushings

A

CT of adrenals +/- MRI, and petrosal sinus sampling of microadenoma

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30
Q

How to screen for complications of cushings syndrome

A

HbA1c, fasting blood sugar, urinalysis, ECG, ECHO, sleep study, colorectal cancer screening, DEXA, vit D, dyslipidaemia

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31
Q

Management of primary cushings

A

laparoscopic adrenalectomy

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32
Q

Management of secondary cushings

A

Transsphenoidal pituitary resection, stereotactic radiotherapy for persistent or recurrent disease, bilateral adrenalectomy (require lifelong supplementation, may cause nelsons syndrome - enlarged pituitary gland / abnormal hormones / invasive adenomas)

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33
Q

Medical therapy to lower cortisol

A

Adrenal enzyme inhibitor (ketoconazole), adrenolytic agent, dopamine agonist (cabergoline), somatostatin analogue (pasirotide), glucocorticoid antagonists (mifepristone)

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34
Q

Pathophysiology of addisons

A

low cortisol

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35
Q

3 key findings of addisons

A
  1. hyperpigmentation. 2. postural BP. 3. electrolyte derangement (low sodium / BLS, high K)
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36
Q

Causes of addisons

A

autoimmune adrenal disease (80%), TB, histoplasmosis, amyloid/sarcoid, bilateral adrenal haemorrhage

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37
Q

Diagnosis of addisons

A

short synacthen test - no increase in plasma cortisol level with ACTH

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38
Q

Management of addisons crisis

A

glucocorticoid stress dosing

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39
Q

Examination of acromegaly

A

hands + cardio + visual fields + thyroid palpate + abdo palpate

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40
Q

Signs of acromegaly

A

enlarged head circumference, hypopituitarism, bilateral hemianopia, macroglossia, obstructed sleep apnea, prominent jaw, gaps between teeth, thyroid nodules, left ventricular hypertrophy, cardiomyopathy, aortic or mitral regurgitation, hypertension, osteoarthrtis, carpel tunnel syndrome, spade like hands, diabetes mellitus, organomegaly, BPH, colonic polyposis, hypogonadism, osteoporosis, peripheral neuropathy

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41
Q

Pathophysiology of acromegaly

A

excessive secretion of growth hormone and thus insulin life growth factor 1.

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42
Q

Causes of acromegaly

A

> 95% are due to somatotroph pituitary adenoma

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43
Q

Mortality of acromegaly

A

> 60% cardiovascular and 25% cancer

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44
Q

Diagnosis of acromegaly

A

serum IGF-1 (high sensitivity), glucose suppression test (growth hormone >1mg/ml 2 post 75g oral glucose), MRI of pituitary

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45
Q

Investigations of acromegaly

A

Reduced cortisol / TSH / T4 / FSH / LH / testosterone. elevated prolactin 25%. Also HbA1c, blood glucose, urinalysis, ECG, ECHO, sleep study, colorectal cancer screening, DEXA, vit D, calcium, dyslipidaemia.

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46
Q

Management of acromegaly.

A
  1. surgical resection - 1st line trans-sphenoid pituitary surgery. 2. Somatostatin analogue (octreotide) - inhibits GH release. 3. Dopamine agonist (cabergoline) for hyperprolactinemia. 4. Growth hormone receptor antagonist (pegvisomant). 5. stereotactic radiotherapy - 40% risk of hypopituitarism. 6. cardiovascular risk reduction
47
Q

Examination for systemic lupus erythematous

A

hands and cardio

48
Q

Presentation for SLE

A

malaise, weight loss, nausea/vomiting, fever, sicca - dry eyes/mouth

49
Q

Signs of SLE

A

delirium, dementia, seizures, psychosis, anaemia, malar butterfly rash (spares nasolabial folds), diffuse photosensitive erythema, discoid rash, alopecia, oral and nasal ulcers, pleurisy, pleural effusions, tenosynovitis, myositis, myalgia, arthralgia, jaccoud’s arthropathy (symmetric, polyarticular, migratory, non-erosive arthritis with correctable deformities), proteinuria, cellular casts, membranous nephropathy, pericarditis, myocarditis, endocarditis, mitral and aortic valve involvement (usually regurg), pulmonary arterial hypertension, accelerated atherosclerosis, haemolytic anaemia, leukopenia, lymphopenia, thrombocytopenia, antiphospholipid antibodies (lupus anticoagulant)

50
Q

Risk factors of SLE

A

procainamide, hydralazine, isoniazid, methyldopa

51
Q

Autoantibodies for SLE

A

ANA sensitive 99.95%, dsDNA specific, anti-RO (sjogrens + neonatal lupus), anti-U1 RNP (myositis overlap), ESR, CRP, compliment

52
Q

Investigations for SLE

A

autoantibodies, Xray (symmetric nonerosive deforming polyarthropathy), renal (uec, urinalysis, proteinuria, casts, sediment +/- biopsy), haem (FBC, low complement correlates with activity, anaemia, low platelets), endocrine (osteoporosis screen), cardiovascular (antiphospholipid antibodies, TTE ?pHTN, exclude coronary artery disease), MRI CNS involvement

53
Q

Non-pharmacological management of SLE

A

smoking cessation, immunisation, exercise

54
Q

Pharmacological management of SLE

A

NSAID - arthralgia. Hydroxychloroquine - skin / joints. Glucocorticoids - flares, also CNS / cardiac / pleural / blood involvement. Maintenance therapy - steroid sparing agent (Azathioprine (after TPMT test) or Methotrexate (with folic acid). Severe disease requires high dose steroids plus immunosuppression with mycophenolate, cyclophosphamide, rituximab, azathioprine, methotrexate. Also management of lupus nephritis, raynuads, antiphospholipid syndrome and osteoporosis.

55
Q

Management of lupus nephritis

A

Mycophenolate, steroid, anti-proteinuric (ACEi/ARB), renal biopsy,

56
Q

Management of raynauds

A

calcium channel blocker (nifedipine as dihydropyridines)

57
Q

Management of antiphospholipid syndrome

A

warfarin

58
Q

Management of OP

A

vit D, calcium, bisphosphonates

59
Q

Examination of scleroderma

A

Hands plus cardio

60
Q

What does CREST stand for

A

calcinosis, Raynaud’s, oesophageal dysfunction, sclerodactyly, telangiectasia

61
Q

Signs of limited scleroderma

A

CREST. bird like facies and restricted oral aperture, telangiectasia of fingers / lips / GIT. Oesophagitis, dysphagia, primary biliary cholangitis, pulmonary arterial hypertension, raynauds, digital ischaemic ulceration, calcinosis, contractions, sclerodactyly (thickening of skin on fingers), functional limitations. Skin thickening is limited to fingers, hands, forearms and lower legs.

62
Q

Signs of diffuse scleroderma

A

Oesophagitis, dysphagia, gastroparesis, GAVE, 30% have ILD (bibasal predominance), renal failure / renal crisis, bird like facies with restricted oral aperture, hypertension, pulmonary hypertension, restrictive cardiomyopathy, pericarditis, reynauds, digital ischaemic ulceration, calcinosis, contractions, sclerodactyly. Skin thickening extends to upper arms, thighs, back, abdomen, trunk and face. Peripheral deforming small joint polyarthritis and tenosynovitis with DIPs affected.

63
Q

Risk factor of scleroderma

A

family history

64
Q

Autoantibodies for scleroderma

A

Centromere - CREST and limited. Scl70/topoisomerase - diffuse and severe lung disease. RNA polymerase 1 and 3 - renal and skin disease. U1 - RNA - overlap with mixed connective tissue disease.

65
Q

Investigations for scleroderma

A

autoantibodies, raised ESR / IgG, anaemia, malabsorption of vitamins ADEK, renal function (crisis occurs early in disease and more common with doses of prednisolone above 15g/day, CXR (reduced lung volumes, reticular interstitial opacities), HRCT (ILD particularly NSIP), respiratory function tests (restrictive picture with reduced TLC / RV / DLCO), ECHO (?pHTN, ?RV failure, restrictive biventricular failure), 6MWT+ABG on room air, endoscope (oesophagitis).

66
Q

Management of Scleroderma

A

General (skin care, cold avoidance, smoking cessation, avoidance of alcohol). Reynauds (dihydropyridine calcium channel blocker, iloprost). Oesophagitis (PPI). Skin (methotrexate or mycophenolate if within 3 years of onset, cyclophosphamide if severe). Arthritis (low dose steroid, hydroxychloroquine). ILD (cyclophosphamide or mycophenolate). Pulmonary Hypertension(endothelin antagonist, PDE5 inhibitor, prostacyclin, riocigent). Renal (ACEi also hypertension). Influenzae and pneumococcal vaccinations. Haemopoietic stem cell transplantation.

67
Q

Examination of Dermatomyositis

A

hands and lung/heart

68
Q

Pathophysiology of dermatomyositis and polymyositis

A

Polymyositis and dermatomyositis are idiopathic inflammatory myopathies with proximal muscle weakness and muscle inflammation. DM has characteristic skin findings. Both carry a risk of solid organ malignancies (cervix, ovarian, lung, bladder, pancreas, stomach).

69
Q

Signs of dermatomyositis

A

Shawl sign, photodistribution erythema, heliotropic reaction (swollen / purple eyelids), oesophageal dysfunction, symmetrical muscle weakness / wasting / tenderness, ILD, cardiac conduction issues, grottans papules, raynauds, small joint symmetrical polyarthritis, scaly rough dry skin, muscle weakness of neck / girdle.

70
Q

Investigations of dermatomyositis

A

Myositis specific auto-antibodies - anti-Jo1. Muscle inflammation markers - CK, LDH, troponin, AST, ALT. Skin biopsy - interface dermatitis. Xray - dystrophic calcification of affected muscles (also consider MRI). Muscle biopsy - both polymyositis and dermatomyositis demonstrate muscle fibre necrosis, degeneration, regeneration and cellular infiltrates. PM = CD8 predominant. DM = CD4 predominant.

71
Q

Management of dermatomyositis

A

Non pharmacological (exercise, aspiration precautions, sun protection). Pharmacological (corticosteroids for induction, azathioprine (post TPMT testing), IVIG for severe disease, hydroxychloroquine for skin disease). Malignancy screening. Management of chronic steroid complications.

72
Q

Key findings for polymyositis

A

Symmetrical proximal weakness (painless) with raised CK/anti Jo. Muscle only.

73
Q

Key findings for induction body myositis

A

Distal hand involvement, wasting, dysphagia, antibody negative, foot drop - ankle / quadriceps / hand / forearm involvement.

74
Q

5 types of HLA-B27 Seronegative Spondyloarthopathies

A
  1. Ankylosing Spondylitis. 2. Reactive Arthritis. 3. Psoriatic Arthritis. 4. IBD-associated Arthritis. 5. Juvenile Idiopathic Arthritis
74
Q

Signs of Ankylosing Spondylitis

A

Anterior uveitis, neck instability, aortic regurgitation, apical lung fibrosis, amyloidosis, autoimmune bowel disease, enthesis Achilles tendon, veritable joint fusion, reduced spinal mobility, modified Schober’s test (>5cm), occiput to wall distance increased, dactylitis (sausage fingers, swelling, PIP), asymmetrical peripheral oligoarthropathies, fixed flexion of hips, decreased chest expansion.

75
Q

Investigations for ankylosing spondylitis

A

Elevated inflammatory markers, negative autoantibodies, HLA-B27, sacral lumbar imaging (xray +/- MRI), CXR, renal function and ECHO before NSAIDs

76
Q

Management of ankylosing spondylitis

A

Non-pharmacological (smoking cessation, exercise, education). Pharmacological (NSAID first line, methotrexate / sulfasalazine for peripheral arthritis, TNF-alpha inhibitors (infliximab) - second line for axial arthritis (remember to exclude HBV + TB), IL-17 inhibitor (secukinumab)).

77
Q

Presentation of ankylosing spondylitis

A

lower back pain with morning stiffness and worse at night. +/- hip/shoulder pain and peripheral joint involvement

78
Q

Risk factors for ankylosing spondylitis

A

family history

79
Q

Diagnosis of ankylosing spondylitis

A
  1. age <45y. 2. >3months of back pain. 3. sacroiliitis (bilateral grade 2 or unilateral grade 3). 4. HLA B27 + two other features (head pain, uveitis, dactylitis, IBD, raised CRP, response to NSAID)
80
Q

Describe the disease and demographics of mixed connective tissue disease

A

Overlap with SLE / SSc / PM and females 20 - 40 years old.

81
Q

Signs of mixed connective tissue disease

A

pulmonary hypertension (main cause of death), ILD, oesophagitis, reynauds, hand and finger oedema, deforming polyarthritis of small joints (like RA)

82
Q

Serum findings of mixed connective tissue disease

A

anti-U1 RNP, ANA + speckled, also monitor renal function

83
Q

xray findings for mixed connective tissue disease

A

erosive deforming polyarthropathy

84
Q

ECHO, cxr and HRCT findings for mixed connective tissue disease

A

ECHO: pulmonary hypertension. CXR + HRCT: basal predominant fibrosis and restrictive lung disease.

85
Q

Management of mixed connective tissue disease

A
  1. Corticosteroids (good response for SLE, poor for SSc). 2. Cyclophosphamide or Rituximab for severe or refractory disease. 3. Pulmonary hypertension management (calcium channel blocker, prostacyclin analogue, endothelin-1 antagonist, PDE5 inhibitor, guanylate cyclase inhibitor). 4. Complications of chronic corticosteroids (diabetes, osteoporosis, hypertension, infections). 5. Management cardiovascular risk factors.
86
Q

Complications of obesity

A

IHD, stroke, OA, diabetes, OSA, NAFLD, hypogonadism, social issues

87
Q

Management of obesity

A

Exercise, diet, bariatric surgery (if BMI >40 or >35 with diabetes or hypertension), liraglutide (GLP-1 analogue) or orlistat (lipase inhibitor)

88
Q

Risk factors and diagnosis of obesity

A

Diagnosis = increased waist circumference, triglycerides, blood pressure, fasting glucose and decreased HDL. Risk factors = family history, medications (anti-psychotics, TCA, steroids, insulin) lifestyle, eating, depression, cushings, thyroid disease

89
Q

Management of hypercalcaemia

A

IVH, bisphosphonates, calcitonin, parathyroidectomies

90
Q

Investigations for hypercalcaemia

A

calcium, vit D, PTH, PTH receptor protein, malignancy screen (CT CAP), 24 hour urine for Familial Hypocalciuric Hypercalcemia

91
Q

Examination for hypercalcaemia

A

neck scar for parathyroid surgery, lymphadenopathy, organomegaly, bradycardia for hypercalcaemia, symptoms of thyrotoxicosis or addisons

92
Q

Symptoms and risk factors for hypercalcaemia

A

Symptoms = fatigue, confusion, constipation, polyuria/polydipsia, muscle/bone aches. Risk factors = history of cancer (b symptoms), history of PTH or CKD (tertiary PTH) or MEN (parathyroid cancer), drug history (thiazide, lithium, vit D, calcium), family history of Familial Hypocalciuric Hypercalcemia.

93
Q

Compare MEN 1, MEN 2A and MEN 2B

A

MEN1 = pituitary adenoma, parathyroid hyperplasia, pancreatic tumour. MEN2A = parathyroid hyperplasia, medullary thyroid carcinoma, pheochromocytoma. MEN2B = mucosal neuromas, marfanoid body habitus, medullary thyroid carcinoma, pheochromocytoma.

94
Q

Describe pathophysiology of renal osteodystrophy

A

Due to increase in phosphate levels due to decreased excretion. Increased parathyroid hormone and FGF-23 - which increases with phosphate excretion. Parathyroid hormone also increases calcium resorption - therefore bones become weaker. FGF-23 also lowers vit D activation, reducing calcium plasma levels.

95
Q

Management of osteoporosis

A

calcium, vit D, bisphosphonate, denosumab (MAB for RANK-L), teripantide (fracture after 1 year of antiresorptive). Also reduce falls risk - rationalise meds, foot wear, eye wear, walking aides, allied health.

96
Q

Indications for bisphosphonates

A

over 70 years old with T <2.5, primary prevention with osteopenia and three months of steroids, minimal trauma fracture

97
Q

Investigations for osteoporosis

A

BMD with DEXA scan, calcium, vit D, PTH, ALP, TFT, investigate myeloproliferative disorder or metastatic cancer in minimal trauma fracture, bone biopsy in osteomalacia

98
Q

Indications for DEXA scan

A

minimal trauma fracture, primary hyperparathyroidism, all women over 65 and men over 70, cushings disease, prolonged steroid use, CKD (renal osteodystrophy)

99
Q

Risk factors for osteoporosis

A

post menopause, elderly, low body weight, inactivity, drugs, alcohol. Hyperthyroidism, steroids, hyperparathyroidism, CKD, gastrectomy, hypogonadism, chronic inflammation. Medications = steroids, PPI, anti-convulsant, CNI, SSRI, alcohol.

100
Q

Diagnosis of diabetes

A

fasting glucose >7 on 2 occasions, HbA1c >6.5%, OGTT >11

101
Q

Presentation of diabetes

A

polyuria, polydipsia, weight loss, infections

102
Q

Secondary causes of diabetes

A

steroids, calcineurin inhibitors, cushings, acromegaly, pancreatic disease

103
Q

Risk factors for diabetes

A

obesity, sedentary lifestyle, EtOH, family history, over 45years old, indigenous, gestational diabetes, PCOS. CV risks = hypertension, hyperlipidaemia, smoking, family history.

104
Q

Investigations for diabetes

A

fasting BSL, HbA1c, insulin, GAD antibodies, c-peptide. T1DM antibodies = glutamine acid decarboxylase, insulin autoantibody, insulinoma associated protein 2, zinc transporter 8.

105
Q

Monitoring for diabetes

A

Frequency? Hypoglycaemia awareness, check pre-drive (if asymptomatic, nil hypos in 6 months, then every 2nd trip), sick day management, insulin to carb ratio (T1DM).

106
Q

Allied health required for diabetes

A

GP, podiatrist, ophthalmologist, dietitian

107
Q

Pharmacological management of diabetes

A

1st line metformin. 2nd line sulfonylurea (beware of hypo). DPP4 inhibitor (sitagliptin). GLP-1 agonist (Lineglutide) use if CCF and obese (causes weight loss. SGLT2 (empagliflozin) - CCH/IHD.

108
Q

Complications of diabetes

A

Episodes of DKA and hypoglycaemia. Microvascular - retinopathy, neuropathy (peripheral, autonomic, sexual), nephropathy (PCR). Macrovascular - cardiac, stroke, peripheral vascular disease (foot ulcer, sexual). Autonomic - orthostatic hypotension, gastroparesis, erectile dysfunction.

109
Q

Autoimmune conditions associated with T1DM

A

vitiligo, thyroid disease, coeliac, pernicious anaemia, Addison’s, autoimmune polyglandular syndrome

110
Q

Acute management of adrenal crisis

A

Steroids (hydrocortisone), fluids (normal saline), electrolyte replacement

111
Q

Confirmation of adrenal crisis

A

Synacthen test

112
Q

Long term management of adrenal crisis, primary verse secondary

A

Primary- hydrocortisone and fludrocortisone
Secondary- hydrocortisone (stress dose when sick)

BPT (11 decks)

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