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41 Cards in this Set
- Front
- Back
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What are the anterior and posterior attachments of the falx cerebri? |
Anterior - cristae galli Posterior - Internal occipital crest |
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What is the contents of the cavernous sinus? |
(i) Trigeminal nerve (Vi) (possibly a bit of Vii) (ii) Oculomotor n., Trochlear n., Abducens n. (iii) Internal carotid artery (iv) Sympathetic plexii (v) Venous blood |
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What nerve is: • A branch of the FACIAL nerve, travels below the trigeminal ganglion • Exits via the foramen lacerum • Travels through the pterygoid canal into the pterygopalatine fossa • Synapses on pterygopalatine ganglion, supplies lacrimal, nasal and palatine glands (tears, mucus) |
Greater petrosal nerve |
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Which nerve is: • A branch of the GLOSSOPHARYNGEAL nerve, (traverses tympanic plexus) travels lateral to the greater petrosal nerve. • Exits via the foramen ovale • Synapses on otic ganglion, supplies parotid gland (saliva). |
Lesser petrosal nerve |
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A 24-year-old man presents with panic symptoms in crowded areas. What would the diagnosis be if the panic attack occurred after: 1• feeling trapped and help not being available: 2• being concerned with what others in the queue were thinking about him 3• bumping into someone who he thought was ‘contaminated’ 4• remembering being at the scene of a hold-up 5• worrying about having to use a lift on his next errand |
Likely diagnosis 1• Pan/Ag 2• Social Phobia 3• OCD 4• PTSD 5• Specific phobia  |
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What is the difference in function of rT3, T3 and T4? |
T3 is 4-5x more potent than T4 rT3 is inert |
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A mutation in which gene can cause auto-immune disease by reducing deletion of self reactive T cells in the thymus? |
AIRE |
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What are the mechanisms of self tolerance? |
1. Deletion of auto-reactive T cells in the thymus 2. Control of activation of T cells - requirement for co-stimulation: CD28-B7 3. Regulatory T cells inhibit auto-reactive T cells |
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Which gene is important for regulation of auto-reactive T cells by regulatory T cells? |
Foxp3 |
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What are the 8 auto-immune diseases in the thyrogastric cluster? |
1. Hypoparathyroidism 2. Thyroiditis 3. Vitiligo 4. Myasthenia gravis 5. Diabetes mellitus 6. Ovarian failure 7. Adrenalitis 8. Pernicious anaemia |
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What are the 7 auto-immune diseases in the lupus cluster? |
1. Rheumatoid arthritis 2. Sjogrens disease 3. Dermatomyositis 4. Scleroderma 5. Myasthenia gravis 6. Chronic active hepatitis 7. SLE |
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What is the target antigen in primary myxoedema? |
TSH-receptor (antibody blocks receptor) |
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What is the target antigen in Graves disease? |
TSH-receptor (antibody stimulates receptor) |
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What is the target antigen in auto-immune (t1) diabetes mellitus? |
Pancreatic islet cell antigens (GAD-65, IA-2) and insulin |
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What is the target antigen in Addison disease? |
Adrenal Cortex Enzymes in steroid biosynthesis (17α hydroxylase & 21-hydroxylase) |
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What is the target antigen in auto-immune hypogonadism? |
Leydig cells (testis) Granulosa, theca cells (ovary) Cytochrome p450 side chain Cleavage enzyme 17α hydroxylase |
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What is the target antigen in auto-immune Hypo-parathyroidism? |
Parathyroid Calcium sensing R (T cells attack receptor, leads to hypocalcaemia) |
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What is the target antigen in pernicious anaemia? |
Gastric parietal cell (intrinsic factor) H+/K+ ATPase (proton pump) |
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What is the target antigen in vitiligo? |
Melanocyte tyrosinase |
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What are the acute and long term adaptations of skeletal muscle for thermogenesis? |
Acute (Shivering): ATP breakdown via “futile” contractions Prolonged: Changes in muscle fibre phenotype; enhanced mitochondrial biogenesis & SERCA (Smooth Endoplasmic Reticulum Ca2+-ATPase) expression |
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Why is brown adipose tissue relevant in adaptive thermogenesis? |
Large numbers of mitochondria, key site of heat generaiton |
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What symptoms result the structural changes of goitre? |
Change in • voice – hoarse: RLN or hypothyroidism • breathing – tracheal compression • swallowing – oesophagus - dysphagia/ odynophagia |
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What are precipitating factors for thyroid disorders? |
• Excess iodine intake (generally hyperthyroidism) – IV iodinated contrast agents (Jod Basedow effect) – Amiodarone (hyper or hypothyroidism) – Kelp tablets • Other – Iodine deficiency (goitre, hypothyroidism) – lithium (goitre ± hypothyroidism) – Interferon (thyroiditis) – Neck irradiation (nodules, hypothyroidism, thyroid cancer) – ? Viruses (subacute thyroiditis) |
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Thyrotoxicosis/ hyperthyroidism signs and symptoms |
HYPERTHYROIDISM: Hair oily/ loss Yuck nails (onycholysis) Poppy Eyes (opthalmopathy, lid retraction in Graves) Reflexes exaggerated Tremor Heart rate up/ Palpitations/ CCF Yawning [fatigability] Restlessness Oligomenorrhea & amenorrhea Intolerance to heat Diarrhea Irritability Sweating Muscle wasting & weight loss |
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Hypothyroidism signs and symptoms |
HYPOTHYROIDISM Hoarse voice Youch - muscle pain and stiffness Periorbital puffiness Oedema (non-pitting/ myxoedema) Too much blood (menorrhagia) Hyporeflexia Yawning (fatigue) Relaxation of reflexes delayed Overweight (weight gain) Intolerance to cold Dry skin and hair tIngling - CTS Slowed HR Movements slow |
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What are the macrovascular complications of diabetes? |
• IHD – may be atypical (SOB, N&V) – Ischemic cardiomyopathy – CCF • CerebroVD – Carotid stenosis, TIA and CVA • PVD – Claudication – Ulceration – Exacerbated by neuropathy and microvascular disease |
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What are the microvascular complications of diabetes? |
1. Eyes - retinopathy, cataracts, glaucoma 2. Nephropathy - microalbinuria, renal impairment 3. Neuropathy - Peripheral (positive or numbness, ulcers) - Autonomic (erectile dysfunction, orthostatic hypotension) |
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What ion transport cycles are involved in thermogenesis? |
1. Futile cycling of Ca++ in SER membrane of skeletal muscle cells - Ca++ leaks out and is actively pumped back in to SER by SERCA 2. Futile cycling of Na - Na+ leak across plasma membrane activates Na+/K+-ATPase to pump them out again 3. Futile cycling of H+ in mitochondria (from intermembrane space to matrix through uncoupling protein) |
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How do mitochondria produce heat? |
Where H+ flux from the intermembrane space to the matrix usually drives ATP synthesis, uncoupling protein provides an alternative route for H+ resulting in futile cycling |
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How is heat production regulated by thyroid hormone? |
1. Increased expression of uncoupling proteins (e.g., UCP-2; UCP-3*) 2. Reduced efficiency of mitochondrial proton pumping 3. Feeding electrons via complex II rather than complex I (less proton pumping)** 4. Thyroid hormone promotes SERCA expression and impairs its efficiency 5. Sympathetic nervous system effects: Enhanced β2-adrenergic receptor expression in muscle |
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What metabolite is measured to determine vitamin D status? |
25(OH) Vitamin D is the major circulating metabolite used to measure vitamin D status 1,25(OH) Vitamin D is the active form, but this is produced in many tissues and 25(OH) is converted to 1,25(OH) (via increased PTH) when levels are low |
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Peter J. is a 6 year old boy who comes to see you. He is being teased at school about being short and his mother is worried. You plot Peter’s height on a growth chart from previous medical records and his height is below 1st percentile and his height velocity is low. After further examination and testing, you conclude that Peter J is a generally healthy child with no obvious cause for impaired growth. What test would you request? |
Growth hormone stimulation test (which uses arginine and insulin to stimulate growth hormone secretion) (Random GH measurements are not useful due to episodic secretion) |
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What are expected normal results from a growth hormone stimulation test? |
a normal response is present if the growth hormone concentrations rise to at least 20mIU/mL at some stage during the test, provided adequate hypoglycemia (< 2.5mmol/L) is achieved. |
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What type of goitre is commonly caused by Hashiotos thyroiditis? |
A non-toxic diffuse or multinodular goitre |
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What type of goitre is commonly caused by Graves disease? |
A diffuse toxic goitre |
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What is the basic mechanism of Hashimotos thyroiditis? |
Activated T cells mainly (Antibodies are of diagnostic importance but unlikely to be pathogenic) --> attack thyroid |
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What is the basic mechanism of primary myxoedema (hypothyroidism)? |
Thyroid blocking auto-antibodies, directed to Thyroid stimulating hormone receptors (TSH-R) --> atrophic thyroiditis |
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What is the basic mechanism of Graves disease? |
Thyroid stimulating auto-antibodies, directed to Thyroid hormone receptors (TSH-R) --> hyperthyroidism |
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What are the currently available anti-thyroid drugs? |
carbimazole and propyl-thiouracil (PTU) |
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carbimazole (AKA Neomercazole (NMZ) ) and propyl-thiouracil (PTU) |
- block the peroxidase activity in the thyroid and prevent the organification of iodide and the coupling of iodotyrosine molecules to form triiodothyronine (T3) and thyroxine (T4). - PTU also has an action on the 5'-deiodinase, one of the actions of which is to convert T4 to T3 - Carbimazole has the advantage of a longer half-life of about 8hrs, while that of PTU is about 2 hrs - Carbimazole is the preferred antithyroid drug in all cases except in the first trimester of pregnancy, or if patients have had side effects |
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How is hypothyroisism treated? |
Thyroxine |
