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Endocrine System > Medicine & Surgery > Flashcards

Medicine & Surgery Flashcards

1
Q

What are the symptoms of a mass effect of the Pituitary Gland?

A

Visual disturbances
–Visual field defect usually very insidious and slowly progressive
–Diplopia
–Visual acuity
*Hydrocephalus
*Headache
*Cranial nerve palsies
*Raised intracranial pressure
* CSF leakage
* Nausea
* Vomitting

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2
Q

What is the term given to excess bleeding into an organ or loss of blood flow to an organ?

A

Apoplexy

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3
Q

What are symptoms of Apoplexy in the Pituitary gland?

A
  • Acute presentation secondary to tumour
    haemorrhagic necrosis
  • Headache
  • Vomiting
  • Blindness
  • Ocular paresis
  • Altered level of consciousness
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4
Q

Excess hormones from the Anterior pituitary gland can cause what diseases?

A
  • Excess GH - —–> Gigantism (children)/Acromegaly (adults) , Organomegaly , Diabetes Mellitus.
  • Excess ACTH —–> Cushing’s syndrome, Diabetes mellitus, osteoporosis, obesity, hypertension.
  • TSH ——-> hyperthyroidism (central) ,cardiac dysrythmia, heat intolerance.
  • Prolactin (PRL) —— > hyperprolactinaemia (galactorrhoea), amenorrhea ( absence of menstruation) , osteoporosis).
  • LH/FSH ——> multiple follicles of ovaries ( asymptomatic) ?
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5
Q

Excess ADH from the pituitary gland can cause what diseases?

A

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) - This causes too much water retention , patient has a low sodium content.

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6
Q

A deficiency in the hormones produced by the Anterior pituitary can cause what diseases?

A
  • LH/FSH —–>hypogonadism
  • GH——-> growth retardation (children)/non-specific (adults) leads to lethargy, anaemia, depression.
  • ACTH——–.>adrenal insufficiency (central)
  • TSH ——–>hypothyroidism (central) - not from thyroid gland but other structures.
  • Prolactin ( Sheehan syndrome- mother not able to breast feed due to infarction of pituitary)
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7
Q

A deficiency in the hormones produced by the Posterior pituitary can cause what diseases?

A
  • Low ADH—-> Central Diabetes Insipidus
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8
Q

What is the examination approach to detect hormone (excess or deficiency)

A

Basal hormonal concentrations -

1. Basal plasma levels (one-time examination)
2. Diurnal dynamics of hormone concentrations (e.g. cortisol)
3. Other hormonal cycles (e.g. menstrual phase dynamics)
4. Urinary output
5. Hormonal metabolites - plasma, urine (e.g. C-peptide)
6. Indirect evaluation - measurement of a metabolic response 	(ADH ... diuresis, insulin ... glycaemia etc.)
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9
Q

What are the functional tests that can be used to detect concentrations of hormones?

A
  • Static testing - no suppression/stimulation
  • Dynamic testing – uses suppression/stimulation
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10
Q

Which functional test should be used if there is a suspected excess of hormone?

A

Suppression test of hormone

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11
Q

Which functional test should be used if there is a suspected deficiency of hormone?

A

Stimulation test of hormone

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12
Q

Give examples of stimulatory tests of pituitary function?

A
  • Insulin hypoglycaemia test
  • Metyrapone test
    *Levodopa test
  • Arginine infusion test
  • TRH test
  • GnRH test
  • CRH test
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13
Q

What is an example of an Inhibitory test for pituitary function?

A

Dexamethasone test

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14
Q

True or False? CT scans are more affordable than MRI scans.

A

TRUE!!

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15
Q

What are the classification of a Pituitary adenoma?

A

Microadenoma LESS than 10mm
Macroadenoma MORE than 10mm (at least 1cm)

lady in lecture say ( large adenoma is 4-5 cm)

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16
Q

Which test can be used in determining Acromegaly?

A

Oral Glucose test

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17
Q

What test can be used to determine Cushing’s syndrome?

A

‐(a)low dose dexamethasone
(b)low dose dexamethasone +CRH
(c)high dose dexamethasone
(d)Inferior petrous sampling + CRH

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18
Q

True or False? Hyperglycemia causes Growth hormone to increase.

A

FALSE!! Hypocgylcemia causes growth hormone to increase

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19
Q

When investigating a pituitary adenoma, which imaging test should be ordered?

A

MRI of the hypophyseal fossa

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20
Q

What infections are common in diabetics?

A
  • Pneumonias & Tuberculosis
  • Pyelonephritis, cystitis, perinephric abscess
  • Soft tissue infections including diabetic foot & osteomyelitis
  • Necrotising fasciitis
  • Mucocutaneous candidiasis
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21
Q

What are infections exclusively in diabetics?

A
  • Invasive ( Malignant) otitis externa
  • Rhinocerebral mucormycosis
  • Emphysematous infections ( pyelonephritis & cholecystitis)
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22
Q

What is the prevalence of Type II diabetes in the Caribbean?

A

Greater than 12%

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23
Q

What are the types of remission of Diabetes?

A

*Partial : Greater than one year of sub-diabetic glycemia

  • Complete : Greater than one year with normoglycemia
  • Prolonged : Complete remission greater than 5 years
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24
Q

What are the features that a patient must present with so they can be screened for diabetes?

A
  • Age&raquo_space; 45
  • Women
  • Obesity
    • waist&raquo_space; 32 inches ( women)
      > 37 inches men
  • BMI > 30kg/m2
  • High blood pressure
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25
Q

What are the causes and associated conditions of Insulin resistance?

A
  • Obesity and inactivity
  • Aging
  • Medications
  • Rare disorders
    *PCOS
    *Atherosclerosis
  • Dyslipidemia
  • Hypertension
  • Type 2 diabetes
  • Genetics
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26
Q

What are the two mechanisms of tissue injury by Hyperglycemia?

A

Glycation pathway
Sorbitol pathway

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27
Q

What are the types of Diabetic Neuropathy?

A
  1. Large fibre neuropathy
  2. Small fibre neuropathy
    3.Proximal motor neuropathy
  3. Acute mono- neuropathy
  4. Entrapment
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28
Q

Microvascular complications of Diabetes are predicted by?

A
  • Duration of diabetes
  • A1c
  • Blood pressure
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29
Q

Macrovascular complications of Diabetes are predicted by?

A
  • Duration of diabetes
  • A1c
  • Blood pressure
  • Blood pressure
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30
Q

What tests should be done on an initial visit if there is suspected diabetes?

A

*Complete examination including BMI/waist
* Retinal exam
*Foot assessment including sensation
* FBG,2hpp,HbA1c
* Fastinglipidpanel
*Serum creatinine and assessment for nephropathy (microalbumin or 24h urine for protein, and creatinine clearance)
ECG or risk stratification if needed

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31
Q

What are the clinical features of diabetes?

A
  • Asymptomatic
  • Polyuria
  • Polydipsia
  • Polyphagia
  • weight loss
  • Blurred vision
  • Lower extremity paresthesias
  • Yeast infections
  • Complications of DM
  • Dry feet , Muscle atrophy
  • Claw toes , ulcer
    *Acanthosis Nigricans ( dirty neck appearance)
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32
Q

What are the anti-inflammatory effects of Cortisol?

A
  • Reduces phagocytic action of white blood cells.
  • Reduces fever
  • Suppresses allergic reactions
  • Wide spread therapeutic use
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33
Q

What is the diagnosis for Cushing syndrome?

A
  • 24 hour urinary cortisol (min 2x)
  • Low dose dexamethasone suppression test (1mg)
  • Midnight salivary cortisol (min 2x)
  • Diurnal rhythm of plasma cortisol
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34
Q

What are the clinical findings in Primary Hyperaldoseronism?

A
  • Hypertension
  • Hypokalemia
  • Sodium retention
  • Muscle weakness
  • Paresthesia - a burning or prickling sensation that is usually felt in the hands, arms, legs, or feet.
    *ECG changes
  • Cardiac decompensation
    *Headaches
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35
Q

What are the causes of Primary Hyperaldosteronism?

A

Aldoseterone secreting tumour
Bilateral hyperplasia of cortex
Rarely carcinoma

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36
Q

True or False? Conn’s syndrome is excess aldosterone secretion INDEPENDENT of the renin-antiogensin system.

A

TRUE!!

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37
Q

What are the screening methods for Hyperaldosteronism ?

A
  • Plasma aldosterone concentration (PAC) and plasma renin activity (PRA).
  • Drawn from ambulant seated patient
  • Morning blood draw
  • Potassium must be normalized (not hypokalemic) to avoid false suppression of aldosterone
  • Positive if Aldosterone-renin ratio (ARR) > 30
    And aldosterone level >15ng/dl
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38
Q

What are examples of Aldosterone suppression tests?

A
  • Iv saline
  • Oral sodium suppression
  • Fludrocortisone suppression test
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39
Q

What is the treatment of Hyperaldosterone?

A

Aldosterone receptor antagonists (spironolactone and eplerenone)- anti hypertensives of choice

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40
Q

What are the symptoms of Pheochrocytoma?

A

Pressure (increase BP)
Pain (headache)
Perspiration
Palpitations (tachycardia) Pallor

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41
Q

What are the rules of the 10’s regarding Pheochromocytoma?

A
  • 10% are malignant
  • 10% are bilateral
  • 10% are extraadrenal in the sympathetic chain (paraganglioma)
  • 10% are in children
  • 10% (actually 30%) are familial (neurofibromatosis, MEN IIa/IIb, von Hippel–Lindau)
  • 10% calcify
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42
Q

What are the symptoms of Primary Adrenal Insufficiency (Addison’s disease)?

A

Fatigue
WEAKNESS
ORTHOSTASIS - decrease in blood pressure after standing
Weight loss
Poor appetite
Neuropsychiatric
Apathy - lack of interest
CONFUSION
Nausea, vomiting
Abdominal pain
SALT craving
HYPERPIGMENTATION ( oral bucosa)
HYPOTENSION
Loss of axillary/pubic hair (women)

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43
Q

What are the laboratory findings for Addison’s disease ( Primary adrenal insufficiency)?

A
  • Hyponatremia
  • Hyperkalemia
  • Hypoglycemia
  • Narrow cardiac silhouette on CXR
  • Low voltage EKG
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44
Q

What are examples of Congenital Adrenal insufficiency?

A
  • Congenital adrenal hyperplasia
  • Wolman disease
  • Adrenal hypoplasia congenita
  • Allgrove syndrome (AAA)
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45
Q

Ambiguous genitalia in females , and precocious puberty in males are major symptoms of?

A

21-Hydroxylase deficiency

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46
Q

In which enzyme deficiency ,can ONLY aldosterone be made?

A

17α-Hydroxylase deficiency.

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47
Q

What levels of cortisol is suggestive of AI ?

A

Less than 3 mcg/dL

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48
Q

What happens to the ACTH levels in adrenal insufficiency?

A

Elevated in adrenal insufficiency

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49
Q

What is the Primary adrenal insufficiency evaluation?

A
  • 0800 cortisol level
  • ACTH level
  • Random cortisol in ill patient
  • ACTH stimulation test
  • Suspected CAH
  • Needs special evaluation
  • Adrenal Autoantibodies
  • ACA—adrenal cortex antibody
  • Anti-21-OH-hydroxylase antibody
50
Q

Fill in the blanks.” Eczema in the acute stage is characterized by ________.”

A

Groups of erythematous vesicles and/or papules .

51
Q

Fill in the blanks.” Eczema in the chronic stage is characterized by ________.”

A

Scaling and lichenification

52
Q

Fill in the blanks.” Eczema in the subacute stage is characterized by ________.”

A

Mainly papules

53
Q

What are Vesicles?

A

Fluid filled lesion less than 0.5 cm. in diameter

54
Q

What are Papules?

A

Solid elevated lesion less than 0.5 cm. in diameter.

55
Q

What is Lichenification?

A

A thickening of the skin with an exaggeration of normal skin markings.

56
Q

In which stage of Eczema is Anacanthosis a dominant feature?

A

Chronic stage

57
Q

In which stage of Eczema is epidermal oedema (spongiosis) most prominent?

A

Acute stage

58
Q

What happens histologically in the subacute stage of Eczema?

A

Spongiosis diminishes and hyperplasia and thickening of the prickle-cell layer (acanthosis) increases.

59
Q

What are the types of Endogenous dermatitis?

A

◦ Atopic dermatitis
◦ Seborrhoeic dermatitis

60
Q

What are the types of Exogenous dermatitis?

A

◦ Irritant contact dermatitis
◦ Allergic contact dermatitis

61
Q

What is Atopic dermatitis?

A

Atopy is said to exist when there is a personal or family history of eczema of a particular distribution, asthma or hay fever (allergic rhinitis).

62
Q

What is the treatment for Atopic Dermatitis?

A
  • Topical and occasionally oral glucocorticoids
  • Calcineurin inhibitors - non-steroidal anti-inflammatory topical agents: ◦ Pimecrolimus cream (Elidel)
    ◦ Tacrolimus ointment (Protopic)
63
Q

What is Psoriasis?

A

A chronic, non-infectious, inflammatory disorder of the skin

64
Q

What are the clinical features of Psoriasis vulgaris?

A

Symmetrical, well-defined, erythematous (red) plaques covered by thick silvery scales.

65
Q

What are the precipitating factors of Psoriasis?

A
  • Streptococcal infection in guttate psoriasis.
  • Drugs:
    ◦ Alcohol
    ◦ Antimalarials
    ◦ Lithium
    ◦ Beta-adrenergic blocking agents
  • HIV infection
66
Q

What are the most common sites for Psoriasis?

A
  • Scalp
  • Extensor aspects of elbows and knees
  • Lower back and sacrum
  • Anterior chest
  • Nails: Thimble pitting, onycholysis, subungual hyperkeratosis
67
Q

Fill in the blanks. “Psoriatic arthropathy commonly affects _______.”

A

The distal interphalangeal joints and the sacroiliac joints.

68
Q

What gene is associated with Psoriatic arthropathy?

A

HLA B27

69
Q

What are the different variations of Psoriasis?

A

Free -Flexural psoriasis
P -Psoriasis vulgaris
P - Pustular psoriasis of palms and soles
E -Erythrodermic psoriasis
G - Guttate psoriasis
G - Generalised pustular psoriasis

” Free Pegg”

70
Q

What is the local (topical) treatment for Psoariasis?

A

C - Coal tar preparations
C- Dithranol
V - Vitamin D analogues
V- Vitamin A analogues
D - Dithranol

71
Q

In regards to the treatment of Psoariasis , which treatment depress DNA synthesis and have an antimitotic effect?

A

Coal tar preparations

72
Q

What is the mechanism of action for Dianthrol?

A

It possesses antiproliferative activity on keratinocytes.

73
Q

Which drug in regards to the treatment of Psoriasis Local (Topical) Treatment normalises keratinization ?

A

Vitamin A analogues

74
Q

Which drug in regards to the treatment of Psoriasis Local (Topical) Treatment have an antiproliferative effect which is mediated by inhibition of DNA synthesis and mitosis?

A

Corticosteroid preparations

75
Q

What is the function of Vitamin D analogues in the treatment of Psoriasis Local ( Tropical ) treatment?

A

They inhibit keratinocyte proliferation and induce terminal differentiation.

76
Q

What drugs are used in the Systemic treatment of Psoriasis?

A
  • Methotrexate inhibits folic acid synthesis during the S phase of mitosis and diminishes .
    epidermal turnover in the lesions of psoriasis.
  • Acitretin is a vitamin A derivative.
  • Cyclosporin A is an immunosuppressant widely used in following organ transplantation.
77
Q

What is Memphis Vulgaris?

A

A serious autoimmune disorder of intraepidermal cell cohesion, resulting in flaccid blisters and painful erosions of the skin and mucous membranes.

78
Q

Psorais Vulgaris is most common in which country?

A

India subcontinent

79
Q

Pemphigus Vulgaris is associated with what gene?

A

HLA- DR4.

80
Q

Pemphigus Vulgaris is most common in what type of people ?

A

Jews

81
Q

What are the clinical features of Pemphigus Vulgaris?

A
  • All skin may be involved.
  • Blisters are flaccid and may arise on normal or erythematous skin.
  • They break easily to leave erosions which are painful.
  • These erosions do not heal spontaneously.
82
Q

Nikolsky’s Sign is common in which disease?

A

Pemphigus Vulgaris

83
Q

What is Nikolsky’s Sign ?

A

This is easy separation of the outer portion of the epidermis from the basal layer on exertion of firm sliding pressure by the finger or thumb.

84
Q

How is Pemphigus Vulgairs diagnosed?

A

The diagnosis may be confirmed by a skin biopsy.

85
Q

The development of Acantholysis (separation of the cells in the prickle cell layer) is seen in what disease?

A

Pemphigus Vulgaris

86
Q

What is the treatment for Pemphigus Vulgaris?

A
  • Glucocorticosteroids( high dose initially) - act by decreasing autoantibody levels.
  • Mycophenolate mofetil

*. Gold

  • Dapsone
  • Plasmapherisis
  • IV immunoglobulin
  • RItuximab
87
Q

What is the Treatment for Grave’s disease?

A

*Antithyroid drugs: propyl-thiouracil, carbimazole
* Radioiodine - I31
* Subtotal thyroidectomy – relapse after antithyroid therapy, pregnancy, severe thyroid eye disease
* Propanolol

88
Q

What is a Thyroid storm?

A

This is a life threatening exacerbation of thyrotoxicosis

89
Q

What is the Treatment for a Thyroid storm?

A

4 P’s:
* Beta blockers (eg, Propranolol)
* Propylthiouracil
* Corticosteroids (eg, Prednisolone),
*Potassium iodide (Lugol iodine)

90
Q

What are the symptoms of a Thyroid storm?

A

Agitation
Delirium
Fever
Diarrhea
Coma
Tachyarrhythmia

91
Q

What is Reidel’s Thyroiditis?

A

Riedel thyroiditis: Very rare disease characterized by painless fibrosis in the thyroid gland and nearby structures in the neck. This can cause tracheal obstruction from the hard, rocklike fibrous deposition

92
Q

What is the radiological diffusion for a Toxic multi nodular goitre?

A

Patchy distribution of radioactive uptake

93
Q

Fill in the blanks. “ If blockage of the Pilosebaceous Canal is SUPERFICIAL _______, ______ &_____ are the results?

A

Comedones, papules and pustules result.

94
Q

True or False? Acne is more common in Males than Females.

A

FALSE!! Unfortunately, it is more common in Females

95
Q

What are the typical lesions associated with acne?

A

Papules
Pustules
Comedones
Nodules
Cysts

96
Q

What contributes to Acne Pathogenesis?

A
  1. Increased production of sebum.
  2. Excessive keratinization at the follicle mouth causing blockage of the pilosebaceous canal.
  3. The presence of micro-organisms.
  4. The production of inflammation.
97
Q

What is the name of the enzyme that aids in the conversation of testosterone?

A

5α reductase

98
Q

What are comedones?

A

Whiteheads + blackheads

99
Q

True or False? Closed comedones are blackheads and open comedones are whiteheads.

A

FALSE!! Open comedones are Black heads
Closed comedones are White heads .
‘ whites are closed ‘ idk lol

100
Q
A
101
Q

Fill in the blanks. “ If blockage of the Pilosebaceous Canal is DEEP _______, ______ &_____ are the results?

A

Nodules, cysts and scarring

102
Q

What are micro-organisms that can cause acne?

A

Propionibacterium acnes – bacteria
Staphylococcus epidermidis – bacteria
Pityrosporum ovale - yeast

103
Q

How does skin bacteria contribitue to the pathogenies of acne?

A
  • Disrupting the follicle wall
  • Causing inflammation
  • Attracting white blood cells
104
Q

What are the common sites for Acne?

A

Forehead
Cheeks
Chin
Nose
Upper chest
Back
Shoulders

105
Q

At what age is Acne vulgarisms at its maximum activity?

A

16 – 18 years

106
Q

When does acne disappear?

A

It does not disappear until early or mid-twenties.

107
Q

True or False? Acne vulgarisms is more common in Teen males than females.

A

TRUE!! ( idk why but its on the slides)

108
Q

What is Infantile acne (milk spots)?

A

This is caused by transplacental stimulation of the sebaceous glands by adrenal androgens.

109
Q

What areas of the body are affected in Nodulocystic acne?

A

The face, chest and back may be affected together or in isolation.

110
Q

What are factors that aggravate acne vulgaris?

A

D- Diet - Foods with high glycemic index such as sweets may aggravate acne.

D- Drugs

E- Endocrine -There may be premenstrual exacerbation.Some oral contraceptives may cause acne to flare

M- Medicaments- Heavy oils, greases
Oily or greasy cosmetics

M- Mechanical trauma (called acne mechanica) - Pressure, friction, rubbing and squeezing from clothing or behavioural habits

I - Industrial

O -Occlusive circumstances -Tight fitting clothes

111
Q

What are some drugs that can aggravate acne ?

A

Hormones: corticosteroids, ACTH, androgens
Halogens: iodides, bromides, chlorides
Antiepileptic drugs: phenobarbitone, phenytoin,
Anti-tuberculosis drugs: Isoniazid, rifampicin

112
Q

What Industrial factors can help to aggravate acne?

A

Halogenated hydrocarbons
Tar
Lubricating oil

113
Q

What are Topical antibiotics used in the treatment of Acne?

A

Clindamycin or erythromycin

114
Q

What are Oral antibiotics used to treat Acne?

A

Oral tetracycline, minocycline, doxycycline, erythromycin

115
Q

What is the Hormone Therapy used to treat Acne?

A

Diane 35, Yasmin

116
Q

What are the adverse effects of Oral retinoid- Isotretinoin (Ro-Accutane)

A

Dry skin and mucosa, teratogenesis, increased liver enzymes, increased serum lipids

117
Q

What drug can be used to treat large inflamed cysts?

A

Intralesional triamcinolone

118
Q

What is Urticaria( Hives or Nettle rash)?

A

Consists of transient itchy red swellings of the skin and mucous membranes. Caused by the release of histamine and other vasoactive agents from granules within the mast cells in blood vessels.

119
Q

What is the duration of Acute urticaria?

A

Less than 6 weeks

120
Q

What is he duration of Chronic urticaria?

A

Lasting greater than 6 weeks

121
Q

What are the treatments for Urticaria?

A
  • Oral antihistamines are the mainstay of treatment.
  • Short courses of corticosteroids may be added if severe or resistant

Endocrine System (10 decks)

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