MRCP p1 incorrects Flashcards
1
Q
What is first-pass metabolism?
A
Metabolism of a drug before it reaches systemic circulation when taken orally, mainly in the liver and intestines.
2
Q
How does first-pass metabolism affect drug bioavailability?
A
Reduces active drug in circulation, requiring higher oral doses or alternative routes (sublingual, IV, transdermal).
3
Q
Name a drug with high first-pass metabolism given sublingually.
A
Glyceryl trinitrate (GTN).
4
Q
What is the mechanism of action of bupropion?
A
Noradrenaline-dopamine reuptake inhibitor (NDRI), reducing nicotine cravings and withdrawal symptoms.
5
Q
Is bupropion an SSRI or MAOI?
A
No, it primarily affects dopamine and noradrenaline, not serotonin.
6
Q
What condition increases aldosterone secretion?
A
Hyponatraemia.
7
Q
What are the main functions of aldosterone?
A
Increases sodium reabsorption, potassium excretion, and water retention.
8
Q
What suppresses aldosterone release?
A
Hypervolaemia, hypokalaemia, and high blood pressure.
9
Q
What occupation is at risk for Brucellosis?
A
Farmers, veterinarians, and abattoir workers.
10
Q
What are key symptoms of Brucellosis?
A
Undulating fever, myalgia, hepatosplenomegaly, and arthritis.
11
Q
What is the causative organism of Brucellosis?
A
Brucella spp. (Gram-negative bacilli).
12
Q
How does bupropion help with smoking cessation?
A
Increases dopamine and noradrenaline, reducing cravings and withdrawal symptoms.
13
Q
How does varenicline differ?
A
Partial nicotine receptor agonist, reducing cravings by blocking nicotine’s effects.
14
Q
What is Holiday Heart Syndrome?
A
Atrial fibrillation triggered by acute alcohol binge, often self-limiting.
15
Q
What is the first-line treatment for stable alcohol-related AF?
A
Rate control with beta-blockers (e.g., esmolol, metoprolol).
16
Q
Why is amiodarone not first choice?
A
Used for rhythm control in structural heart disease or persistent AF, not self-limiting cases.
17
Q
Which TB patient requires prolonged respiratory isolation?
A
Multi-drug-resistant, smear-positive pulmonary TB.
18
Q
When can fully sensitive TB patients come out of isolation?
A
After 2 weeks of treatment if no longer coughing and smear-negative.
19
Q
What is the first-line antibiotic for Chlamydia pneumoniae?
A
Macrolides (e.g., clarithromycin, azithromycin).
20
Q
Why are beta-lactams ineffective for Chlamydia?
A
Chlamydia lacks a peptidoglycan cell wall, which beta-lactams target.
21
Q
Why does GTN require a lower dose than oral isosorbide mononitrate?
A
GTN is given sublingually to bypass first-pass metabolism, whereas isosorbide mononitrate undergoes extensive hepatic metabolism.
22
Q
What routes bypass first-pass metabolism?
A
Sublingual, intravenous, transdermal, intramuscular, and subcutaneous.
23
Q
Why is lidocaine not given orally?
A
It undergoes extensive first-pass metabolism, making it ineffective.
24
Q
What is gestational thrombocytopenia?
A
A benign condition where platelet count decreases in pregnancy, usually mild and asymptomatic.
25
How is gestational thrombocytopenia diagnosed?
Diagnosis of exclusion; occurs in the third trimester with a platelet count >70,000 without other signs of disease.
26
Does gestational thrombocytopenia require treatment?
No, it typically resolves postpartum without treatment.
27
What is the most common cause of thrombocytopenia in pregnancy?
Gestational thrombocytopenia.
28
When is treatment required for thrombocytopenia in pregnancy?
If platelet count <50,000 or associated with preeclampsia, HELLP syndrome, or ITP.
29
What is the treatment for immune thrombocytopenic purpura (ITP) in pregnancy?
First-line: Corticosteroids or IVIG. Second-line: Splenectomy if refractory.
30
What is Cushing’s syndrome?
A condition caused by prolonged exposure to high levels of cortisol.
31
What are common causes of Cushing’s syndrome?
Exogenous steroids (most common), pituitary adenoma (Cushing’s disease), adrenal tumors, or ectopic ACTH secretion.
32
What differentiates Cushing’s disease from Cushing’s syndrome?
Cushing’s disease is specifically caused by a pituitary adenoma secreting excess ACTH.
33
What is the diagnostic test for Cushing’s syndrome?
24-hour urinary free cortisol, low-dose dexamethasone suppression test, or late-night salivary cortisol.
34
What is osteoporosis?
A disease characterized by decreased bone density and increased fracture risk.
35
What are common risk factors for osteoporosis?
Postmenopausal status, aging, steroid use, low calcium/vitamin D, smoking, alcohol, and inactivity.
36
What is the first-line treatment for osteoporosis?
Bisphosphonates (e.g., alendronate), calcium, vitamin D, and weight-bearing exercise.
37
What is Wilson’s disease?
An autosomal recessive disorder causing copper accumulation in the liver and brain due to defective ceruloplasmin function.
38
What are key clinical features of Wilson’s disease?
Hepatic dysfunction, neurological symptoms (tremors, ataxia, dystonia), psychiatric disturbances, and Kayser-Fleischer rings.
39
What is the treatment for Wilson’s disease?
Copper chelation therapy with penicillamine or trientine, and zinc to reduce copper absorption.
40
What are the stages of normal wound healing?
Inflammation (0-3 days), proliferation (4-21 days), and remodeling (up to 1 year).
41
What occurs during the proliferation phase?
Fibroblast migration, collagen deposition, angiogenesis, and epithelialization.
42
What is the role of collagen in wound healing?
Collagen provides structural integrity, with type III collagen initially deposited, later replaced by type I collagen.
43
What is the mode of transmission for Hepatitis A?
Fecal-oral route, often through contaminated food or water.
44
Is Hepatitis A acute or chronic?
Acute only; it does not cause chronic infection.
45
What is the key marker for recent Hepatitis A infection?
Anti-HAV IgM.
46
What are the key markers for Hepatitis B infection?
HBsAg (active infection), Anti-HBc IgM (acute), Anti-HBc IgG (chronic or past), Anti-HBs (immunity).
47
How is Hepatitis B transmitted?
Bloodborne, sexual, perinatal (mother to child).
48
What is the main mode of transmission of Hepatitis C?
Bloodborne, primarily through IV drug use, needlestick injuries, and transfusions before 1992.
49
What is the key test for active Hepatitis C infection?
HCV RNA (viral load).
50
Can Hepatitis C be cured?
Yes, direct-acting antivirals (e.g., sofosbuvir, ledipasvir) achieve >95% cure rates.
51
What is hyperprolactinemia?
A condition where prolactin levels are abnormally high, often due to dopamine inhibition.
52
How do dopamine antagonists cause hyperprolactinemia?
They block dopamine receptors (D₂) in the pituitary, removing dopamine’s inhibitory effect on prolactin release.
53
Which antipsychotics cause hyperprolactinemia?
Typical (haloperidol, chlorpromazine, fluphenazine) and some atypicals (risperidone, amisulpride, sulpiride).
54
Which anti-emetics cause hyperprolactinemia?
Metoclopramide and domperidone, due to their D₂ antagonist activity.
55
Which antihypertensive drug can cause hyperprolactinemia?
Methyldopa (reduces dopamine synthesis).
56
Which antidepressants can cause hyperprolactinemia?
SSRIs (fluoxetine, sertraline, paroxetine), TCAs (amitriptyline), and MAOIs (phenelzine, tranylcypromine).
57
How do opioids increase prolactin?
They suppress dopamine release, reducing its inhibitory effect on prolactin secretion.
58
Which recreational drug is associated with hyperprolactinemia?
Cannabis.
59
Which hormonal medications can increase prolactin?
Oral contraceptives (estrogens) and high-dose progestins (e.g., medroxyprogesterone).
60
What test confirms hyperprolactinemia?
Serum prolactin levels, ideally measured in the morning after fasting.
61
What is the first-line treatment for drug-induced hyperprolactinemia?
Discontinuation of the offending drug if possible or switching to an alternative with a lower risk.
62
What medications can be used to treat hyperprolactinemia?
Dopamine agonists such as bromocriptine or cabergoline.
63
What is Paget's disease of bone?
A chronic disorder causing abnormal bone remodeling, leading to enlarged, weak, and deformed bones.
64
Who is most commonly affected by Paget’s disease?
Older adults, typically >55 years, more common in men.
65
What is the primary defect in Paget’s disease?
Excessive bone resorption by hyperactive osteoclasts followed by disorganized bone formation by osteoblasts.
66
Which bones are most commonly affected?
Pelvis, skull, spine, femur, tibia.
67
What are the main symptoms of Paget’s disease?
Bone pain, skeletal deformities (e.g., bowed legs), fractures, and hearing loss if skull is involved.
68
What is the key laboratory marker for Paget’s disease?
Elevated alkaline phosphatase (ALP) with normal calcium and phosphate levels.
69
What are typical X-ray findings in Paget’s disease?
Thickened, sclerotic bone with a 'cotton wool' appearance in the skull.
70
What are potential complications of Paget’s disease?
Pathological fractures, osteoarthritis, hearing loss, high-output heart failure, osteosarcoma (rare).
71
What imaging is used to confirm Paget’s disease?
X-ray (first-line), bone scan for disease extent, MRI/CT for complications.
72
What is the first-line treatment for symptomatic Paget’s disease?
Bisphosphonates (e.g., zoledronic acid, alendronate) to inhibit osteoclast activity.
73
When is treatment recommended in Paget’s disease?
If symptomatic, high-risk fracture sites, or elevated ALP with active disease on imaging.
74
What is used to monitor treatment response?
Serial alkaline phosphatase (ALP) levels.
75
What is CAIS?
A genetic disorder where individuals with a 46,XY karyotype are resistant to androgens, leading to a female phenotype despite having testes.
76
What is the genetic cause of CAIS?
Mutations in the androgen receptor (AR) gene on the X chromosome.
77
What are the typical hormone levels in CAIS?
High testosterone (male range), high luteinizing hormone (LH), and normal/elevated estrogen.
78
What are the key clinical features of CAIS?
Female external genitalia, absent uterus and ovaries, undescended testes (often in the inguinal canal), primary amenorrhea, and lack of pubic/axillary hair.
79
How is CAIS diagnosed?
Karyotype (46,XY), high testosterone levels, androgen receptor gene testing, and imaging (USS/MRI to confirm absent uterus and undescended testes).
80
What conditions should be considered in the differential for CAIS?
Müllerian agenesis (Mayer-Rokitansky-Küster-Hauser syndrome), Swyer syndrome, 5-alpha reductase deficiency.
81
What is the management of CAIS?
Gonadectomy (after puberty to allow feminization), hormone replacement therapy (estrogen), psychological support, and gender identity counseling.
82
What are the long-term health concerns in CAIS?
Increased risk of gonadal tumors (e.g., gonadoblastoma if testes are retained), osteoporosis due to lack of androgen activity, and psychosocial issues.
83
What autoantibody is associated with rheumatoid arthritis?
Rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies.
84
85
What is first-pass metabolism?
It is the metabolism of a drug before it reaches systemic circulation when taken orally, primarily occurring in the liver and intestines.
86
How does first-pass metabolism affect drug bioavailability?
It reduces the active drug that reaches circulation, requiring higher oral doses or alternative routes (e.g., sublingual, IV, transdermal).
87
Name a drug with high first-pass metabolism that is given sublingually to avoid this effect.
Glyceryl trinitrate (GTN).
88
What is the mechanism of action of bupropion (Zyban)?
It is a noradrenaline-dopamine reuptake inhibitor (NDRI) that reduces nicotine cravings and withdrawal symptoms.
89
Is bupropion an SSRI or MAOI?
No, it primarily affects dopamine and noradrenaline, not serotonin.
90
What condition increases aldosterone secretion?
Hyponatraemia.
91
What are the main functions of aldosterone?
Increases sodium reabsorption, potassium excretion, and water retention to regulate blood pressure.
92
What suppresses aldosterone release?
Hypervolaemia, hypokalaemia, and high blood pressure.
93
What occupation is at risk for Brucellosis?
Farmers, veterinarians, and abattoir workers.
94
What are key symptoms of Brucellosis?
Undulating fever, myalgia, hepatosplenomegaly, and arthritis.
95
What is the causative organism of Brucellosis?
Brucella spp. (Gram-negative bacilli).
96
What is essential thrombocythemia (ET)?
A myeloproliferative disorder characterized by an overproduction of platelets due to a clonal proliferation of megakaryocytes.
97
What are the main clinical features of ET?
Thrombosis (arterial and venous), bleeding (if platelets are dysfunctional), headaches, dizziness, and erythromelalgia (burning pain and redness in extremities).
98
What genetic mutation is commonly associated with ET?
JAK2 mutation (in ~50-60% of cases), CALR or MPL mutations in others.
99
What is the primary treatment for ET?
Low-dose aspirin for all patients; cytoreductive therapy (e.g., hydroxyurea, anagrelide) for high-risk patients.
100
What are the major complications of ET?
Thrombosis, hemorrhage, and transformation into myelofibrosis or acute leukemia.
101
What is aphasia?
A language disorder caused by brain damage, affecting speech, comprehension, reading, or writing.
102
What is the most common cause of aphasia?
Stroke, particularly affecting the dominant (usually left) hemisphere.
103
What are the main types of aphasia?
Broca’s aphasia, Wernicke’s aphasia, global aphasia, conduction aphasia, anomic aphasia, and transcortical aphasias.
104
What is Broca’s aphasia?
A non-fluent aphasia with impaired speech production but relatively preserved comprehension.
105
What brain region is affected in Broca’s aphasia?
Broca’s area in the left inferior frontal gyrus.
106
How do patients with Broca’s aphasia communicate?
They use short, effortful speech with agrammatism but good understanding.
107
What is Wernicke’s aphasia?
A fluent aphasia with impaired comprehension and meaningless speech (word salad).
108
What brain region is affected in Wernicke’s aphasia?
Wernicke’s area in the left superior temporal gyrus.
109
Do patients with Wernicke’s aphasia have awareness of their deficit?
No, they often lack insight into their condition.
110
What is global aphasia?
A severe form of aphasia where both speech production and comprehension are impaired.
111
What causes global aphasia?
Large left hemisphere stroke affecting both Broca’s and Wernicke’s areas.
112
Can patients with global aphasia improve?
Some recovery is possible with therapy, but severe cases have persistent deficits.
113
What is conduction aphasia?
A fluent aphasia with impaired repetition but intact comprehension.
114
What brain structure is damaged in conduction aphasia?
The arcuate fasciculus, which connects Broca’s and Wernicke’s areas.
115
What is the hallmark feature of conduction aphasia?
Difficulty repeating phrases despite good comprehension and fluent speech.
116
What is anomic aphasia?
A mild form of aphasia characterized by word-finding difficulties.
117
How do patients with anomic aphasia communicate?
They speak fluently but struggle to find the right words, often circumlocuting (describing instead of naming).
118
What causes anomic aphasia?
Various brain lesions, including stroke, trauma, or neurodegenerative diseases.
119
What are the types of transcortical aphasias?
Transcortical motor, transcortical sensory, and mixed transcortical aphasia.
120
What is unique about transcortical aphasias?
Repetition is preserved, unlike in Broca’s or Wernicke’s aphasia.
121
What is transcortical motor aphasia?
Similar to Broca’s aphasia but with intact repetition.
122
What is transcortical sensory aphasia?
Similar to Wernicke’s aphasia but with preserved repetition.
123
What is mixed transcortical aphasia?
A severe form where both speech production and comprehension are impaired, but repetition is intact.
124
How is aphasia diagnosed?
Bedside language assessment, formal tests (e.g., Western Aphasia Battery), and neuroimaging (CT/MRI) to identify lesions.
125
Why is MRI preferred for aphasia assessment?
It provides detailed brain imaging to locate strokes or lesions affecting language areas.
126
What other conditions should be ruled out when evaluating aphasia?
Dysarthria, apraxia of speech, dementia, and psychiatric disorders.
127
What is the main treatment for aphasia?
Speech and language therapy to improve communication skills.
128
Can aphasia be cured?
Some patients recover spontaneously, but many require long-term therapy.
129
What aids can help aphasic patients communicate?
Augmentative communication devices, gestures, and visual aids.
130
What is Tuberous Sclerosis?
A genetic disorder characterized by benign tumors affecting multiple organs, including the brain, skin, kidneys, heart, and lungs.
131
What are the two disease-causing genes in Tuberous Sclerosis?
TSC1 (chromosome 9q34, encodes hamartin) and TSC2 (chromosome 16p13, encodes tuberin).
132
What is the function of hamartin and tuberin?
Both act as tumor suppressor proteins, regulating cell growth and proliferation.
133
How is Tuberous Sclerosis inherited?
Autosomal dominant, though about 60% of cases arise from new mutations.
134
Which gene mutation is associated with more severe mental disability?
TSC2 mutation.
135
What are the common dermatological features?
Facial angiofibromas (adenoma sebaceum), Ash leaf-shaped macules (hypopigmented), Shagreen patches, Depigmented naevi, Café-au-lait spots, Sublingual fibromas.
136
What are the major neurological symptoms?
Infantile spasms, Seizures, Hydrocephalus (due to cerebral glial nodules).
137
What eye abnormalities are seen in Tuberous Sclerosis?
Retinal hamartomas (phakomas), Hypopigmented iris spots, Chromatic retinal patches.
138
What is the most common cardiac tumor in Tuberous Sclerosis?
Rhabdomyomas.
139
What are the common tumors seen in Tuberous Sclerosis?
Renal angiomyolipomas (bilateral), Wilms’ tumor, Cardiac and olfactory hamartomas, Ependymomas, Astrocytomas.
140
What are other systemic features of Tuberous Sclerosis?
Renal cysts, Hypertension, Aortic aneurysm.
