Drugs Causing Pseudotumor cerebri

1. Hypervitaminosis A

2. Oral contraceptives

3. Tetracyclines

4. Glucocorticoids ( withdrawal )

5. Amiodarone

6. Mineralocorticoids ( withdrawal )

Drugs causing pancreatitis

Definite Cause :

1. 5-Aminosalicylate
2. 6-Mercaptopurine
3. Azathioprine
4. Cytosine arabinoside
5. Dideoxyinosine
6. Diuretics
7. Estrogens
8. Furosemide
9. Metronidazole
10. Pentamidine
11. Tetracycline
12. Thiazide
13. Trimethoprim-sulfamethoxazole
14. Valproic acid

Probable Cause :

1. Acetaminophen
2. α-Methyl-DOPA
3. Isoniazid
4. l-Asparaginase
5. Phenformin
6. Procainamide
7. Sulindac

 ( DOPA, dihydroxyphenylalanine )

P.S : This question is very frequently asked in PGI chandigarh entrance examination .

Drugs causing Parkinsonism

Here is a list of drugs and toxins causing parkinsonism :

1. Fluoxetine
2. Valproate
3. Alpha methyl dopa
4. Neuroleptics
5. Dopamine depleting agents
6. Anti-emetics
7. Lithium carbonate
8. Some selective anti-psychotics

Toxins which cause parkinsonism are :

1. CO ( carbonmonoxide )
2. Cyanide
3. CS2
4. Manganese
5. Methanol
6. MPTP
7. N-Hexane

Antimicrobial chemotherapy - Cell wall synthesis inhibitors

		AGENT Cycloserine	SITE OF ACTION      Peptidoglycan tetrapeptide side chain	EFFECT     Bactericidal
		Phosphomycin	Formation of N-acetylmuramic acid	Bactericidal
		Bacitracin	Membrane carrier molecule	Bactericidal
		Penicillins	Peptidoglycan cross-linking	Bactericidal
		Cephalosporins carbapenems	,     Peptidoglycan cross-linking	Bactericidal
		Vancomycin	Translocation of cell wall   intermediates	Bactericidal

Antimicrobial chemotherapy - Protein biosynthesis inhibitors

Streptomycin	30S ribosomal subunit	Bactericidal
Gentamicin	30S ribosomal subunit	Bactericidal
Tetracycline	30S ribosomal subunit	Bacteriostatic
Spectinomycin	30S ribosomal subunit	Bacteriostatic
Chloramphenicol	50S ribosomal subunit	Bacteriostatic
Erythromycin	50S ribosomal subunit	Bacteriostatic
Clindamycin	50S ribosomal subunit	Bacteriostatic
Griseofulvin	Microtubule function	Fungistatic

Drugs causing Fatty liver

1. Antiarrythmics - Amiodarone

2. Antibiotic - Tetracycline ( high-dose, intravenous )

3. Anticonvulsant - Valproic acid

4. Antiviral - Dideoxynucleosides ( eg: Zidovudine ), protease inhibitors ( indinavir, ritonavir )

5. Oncotherapeutics - Asparginase, Methotrexate .

Monoclonal antibodies approved for Hematological and Solid tumors

ANTIGEN AND TUMOR CELL TARGETS	ANTIGEN FUNCTION	NAKED ANTIBODIES
Antigen: CD20	Proliferation/differentiation	Rituximab (chimeric)
Tumor type: B-cell lymphoma and CLL
Antigen: CD52	Unknown	Alemtuzumab (humanized)
Tumor type: B-cell CLL and T-cell lymphoma
Antigen: CD25 alpha subunit	Activation antigen	Daclizumab (humanized)
Tumor type: T-cell mycosis fungoides
Antigen: CD33	Unknown	Gemtuzumab (humanized)
Tumor type: acute myeloid leukemia
Antigen: HER2/neu (ErbB-2)	Tyrosine kinase	Trastuzumab (humanized)
Tumor type: breast cancer
Antigen: EGFR (ErbB-1)	Tyrosine kinase	Cetuximab (chimeric)
Tumor type: colorectal; NSCLC; pancreatic, breast
Antigen: VEGF	Angiogenesis	Bevacizumab (humanized)
Tumor type: colorectal cancer

Drugs causing Megaloblastic anemia

1. Phenytoin (anticonvulsant)

2. Primidone (anticonvulsant)

3. Phenobarbitone (anticonvulsant)

4. Sulfasalazine

5. Nitrous oxide
6. Folate antagonists (inhibitors of Dihydrofolate reductase) like Methotrexate, Pentamidine,     Pyrimethamine, Triamterene, Trimethoprim and Cotrimoxazole.
7. Drugs that inhibit DNA synthesis may cause Megaloblastic anemia
    example : 6a. Purine antagonists = 6-Mercaptopurine, Azathioprine.
                   6b. Pyramidine antagonists = 5 FU, Cytosine arabinoside .

                   6c. Others = Hydroxyurea, acyclovir and zidovudine (AZT, Azidothymidine).
8. Nitrofurantoin (less well documented)
9. Tetracycline (less well documented)
10. Anti-Tuberculosis drugs (less well documented)

Characteristics of antituberculous drugs

Drug Most Common Side Effects Tests for Side Effects Drug Interactions Isoniazid- Bactericidal to both extracellular and intracellular organisms. Pyridoxine, 10 mg orally daily as prophylaxis for neuritis; 50–100 mg orally daily as treatment. Peripheral neuropathy, hepatitis, rash, mild CNS effects. AST and ALT; neurologic examination. Phenytoin (synergistic); disulfiram. Rifampin- Bactericidal to all populations of organisms. Colors urine and other body secretions orange. Discoloring of contact lenses. Hepatitis, fever, rash, flu-like illness, gastrointestinal upset, bleeding problems, renal failure. CBC, platelets, AST and ALT. Rifampin inhibits the effect of oral contraceptives, quinidine, corticosteroids, warfarin, methadone, digoxin, oral hypoglycemics; aminosalicylic acid may interfere with absorption of rifampin. Significant interactions with protease inhibitors and nonnucleoside reverse transcriptase inhibitors. Pyrazinamide- Bactericidal to intracellular organisms. Hyperuricemia, hepatotoxicity, rash, gastrointestinal upset, joint aches. Uric acid, AST, ALT. Rare. Ethambutol- Bacteriostatic to both intracellular and extracellular organisms. Mainly used to inhibit development of resistant mutants. Use with caution in renal disease or when ophthalmologic testing is not feasible Optic neuritis (reversible with discontinuance of drug; rare at 15 mg/kg); rash. Red-green color discrimination and visual acuity (difficult to test in children under 3 years of age). Rare. Streptomycin- Bactericidal to extracellular organisms. Use with caution in older patients or those with renal disease. Eighth nerve damage, nephrotoxicity. Vestibular function (audiograms); BUN and creatinine. Neuromuscular blocking agents may be potentiated and cause prolonged paralysis.

AST, aspartate aminotransferase; ALT, alanine aminotransferase; CBC, complete blood count; BUN, blood urea nitrogen.

Drugs causing CYP3A inhibition

1. HIV antivirals : Indinavir, nelfinavir, ritonavir, Saquinavir
2. Clarithromycin
3. Itraconazole and Ketaconazole
4. Nefazodone
5. Telithromycin
6. Aprepitant
7. Erythromycin
8. Grapefruit juice
9. verapamil, diltiazem
10. Cimetidine
11. Amiodarone
12. Chloramphenicol
13. Ciprofloxacin
14. Delaviridine
15. Diethyl-dithiocarbamate
16. fluvoxamine
17. gestodene
18. Imatinib
19. Mibefradil
20. Mifepristone
21. Norfloxacin
22. Norfluoxetine
23. Starfruit
24. Voriconazole

Beta blockers

*Beta blockers are drugs which act against the beta adrenergic receptors. There are three kinds of adrenergic receptors namely beta1, beta2 and beta3.

*First generation beta blockers (non-selective beta blockers) :
- Propranolol
- Nadolol
- Timolol
- Penbutalol
- Pindolol
- Oxprenolol
- Alprenolol

*Second generatin beta blockers ( Beta1 selective beta blockers = Cardioselective beta blockers ):
- Acebutalol
- Celiprolol
- Bisoprolol
- Metaprolol
- Nebivolol (most cardioselective beta blocker)
- Atenolol
- Esmolol
- Betaxolol

*Third generation beta blockers ( These are beta blockers which have additional vasodilator property ):
- Labetalol and Carvedilol ( act as vasodilators by antagonising alpha1 receptors on blood vessels)
- Tilosolol ( act as vasodilator by opening up potassium channels)
- Nebivolol and Nipradilol ( generate Nitric oxide )
- Bevantolol, Betaxolol, Carvedilol ( inhibit calcium channels )
- Bopindolol, Carteolol, Celiprolol ( agonists of beta2 receptors )

* Beta blockers with Membrane stabilising activity (local anaesthetic activity) :
- Propranolol (most effective)
- Labetalol
- Acebutolol
- Metaprolol
- Pindolol

* Beta blockers with intrinsic sympathomimetic activity :
- Oxprenolol
- Alprenolol
- Pindolol
- Celiprolol

* Beta blockers which are lipid insoluble ( so they are excreted by kidney and hence contraindicated in renal failure - LONG ACTING AGENTS ) :
- Nadolol
- Sotalol
- Acebutalol
- Atenolol
- Betaxolol
- Bisoprolol
- Celiprolol

* Longest acting beta blocker is Nadolol
* Shortest acting beta blocker is esmolol.

Endometrial carcinoma - FIGO staging

The International Federation of Gynecology and Obstetrics (FIGO) staging system for carcinoma of corpus uteri is as follows:

• Stage IA - Tumor limited to endometrium
• Stage IB - Invasion to less than one half the myometrium
• Stage IC - Invasion to more than one half the myometrium
• Stage IIA - Endocervical glandular involvement only
• Stage IIB - Cervical stromal invasion
• Stage IIIA - Tumor invades serosa and/or adnexa and/or positive peritoneal cytology.
• Stage IIIB - Vaginal metastasis
• Stage IIIC - Metastases to pelvic and/or para-aortic lymph nodes
• Stage IVA - Tumor invasion of bladder and/or bowel mucosa
• Stage IVB - Distant metastases including intra-abdominal and/or inguinal lymph nodes.

Absolute contraindications of oral contraceptive pills

1. carcinoma of breast and genitals
2. congenital hyperlipidemia
3. porphyria
4. cardiac abnormalities
5. moderate to severe hypertension
6. previous or present history of thromboembolism
7. undiagnosed abnormal uterine bleeding
8. impending major surgery to avoid post operative thromboembolism
9. liver diseases , hepatoma or history of jaundice during past pregnancy

Endometrial Cancer Risk Factors

Proliferation of the endometrium is under the control of estrogen, and prolonged exposure to unopposed estrogen from either endogenous or exogenous sources plays a central etiologic role. Risk factors for endometrial cancer include obesity, low fertility index, early menarche, late menopause, and chronic anovulation. Granulosa cell tumors of the ovary that secrete estrogen may present with synchronous endometrial cancers. Chronic unapposed estrogen replacement increases the risk, and women taking tamoxifen for breast cancer treatment or prevention have a twofold increased risk.

The Lynch syndrome occurs in families with an autosomal dominant mutation of mismatch repair genes MLH1, MSH2, MSH6, and PMS2, which predispose to nonpolyposis colon cancer as well as endometrial and ovarian cancer. The estimated lifetime risk for endometrial cancer is 40–60%, with a mean age around 50 years. Unlike colorectal cancer, endometrial cancer risk is not lower in MSH6 mutation carriers. Most women present with stage I disease, and the survival rate is generally good (5-year survival 88%). No unique endometrial screening strategies have been established for Lynch family gene carriers.

• Obesity

• Impaired carbohydrate tolerance

• Nulliparity

• Late menopause

• Unopposed oestrogen therapy

• Functioning ovarian tumours

• Previous pelvic irradiation

• Family history of carcinoma of breast, ovary

or colon

Drugs Whose Effectiveness Is Influenced by Combination Oral Contraceptives

Interacting Drug Documentation Management Analgesics       Acetaminophen Adequate Larger doses of analgesic may be required   Aspirin Probable Larger doses of analgesic may be required   Meperidine Suspected Smaller doses of analgesic may be required   Morphine Probable Larger doses of analgesic may be required Anticoagulants       Dicumarol, warfarin Controversial   Antidepressants       Imipramine Suspected Decrease dosage about a third Tranquilizers       Diazepam, alprazolam Suspected Decrease dose   Temazepam Possible May need to increase dose   Other benzodiazepines Suspected Observe for increased effect Anti-inflammatories       Corticosteroids Adequate Watch for potentiation of effects, decrease dose accordingly Bronchodilators       Aminophylline, theophylline, caffeine Adequate Reduce starting dose by a third Antihypertensives       Cyclopenthiazide Adequate Increase dose   Metoprolol Suspected May need to lower dose Other       Troleandomycin Suspected liver damage Avoid   Cyclosporine Possible May use smaller dose   Antiretrovirals Variable See manufacturer or other

Drugs that May Reduce Combined Hormonal Contraceptive Efficacy

Interacting Drug Documentation Antituberculous     Rifampin Established; reduced efficacy if 50 microg EE Antifungals     Griseofulvin Strongly suspected Anticonvulsants and sedatives     Phenytoin, mephenytoin, phenobarbital, primidone, carbamzepine, ethosuximide Strongly suspected; reduced efficacy if 50 microg EE; trials lacking Antibiotics     Tetracycline, doxycycline Two small studies find no association   Penicillins No association documented   Ciprofloxacin No effect on efficacy of a 30 microg EE + desogestrel pill   Ofloxacin No effect on efficacy of a 30 microg EE + levonorgestrel pill Antiretrovirals Variable effects; see manufacturer or other

EE = ethinyl estradiol.

Vasopressin Receptors

*The cellular effects of vasopressin (ADH) are mediated mainly by interactions of the hormone with the three types of receptors, V_1a, V_1b, and V₂.

*The V_1a receptor is the most widespread subtype of Vasopressin receptor; it is found in vascular smooth muscle, the adrenal gland, myometrium, the bladder, adipocytes, hepatocytes, platelets, renal medullary interstitial cells, vasa recta in the renal microcirculation, epithelial cells in the renal cortical collecting-duct, spleen, testis, and many CNS structures.

*V_1b receptors have a more limited distribution and are found in the anterior pituitary, several brain regions, the pancreas, and the adrenal medulla.

*V₂ receptors are located predominantly in principal cells of the renal collecting-duct system but also are present on epithelial cells in the thick ascending limb and on vascular endothelial cells.

*Although originally defined by pharmacological criteria, vasopressin receptors now are defined by their primary amino acid sequences.

*The cloned vasopressin receptors are typical heptahelical G protein–coupled receptors.

*Manning and coworkers (1999) have synthesized novel hypotensive vasopressin peptide agonists that do not interact with V_1a, V_1b, or V₂ receptors and may stimulate a putative vasopressin vasodilatory receptor. Finally, two additional putative receptors for vasopressin have been cloned.

*A vasopressin-activated Ca²⁺-mobilizing receptor with one transmembrane domain binds vasopressin and increases intracellular Ca²⁺. A dual angiotensin II–vasopressin heptahelical receptor activates adenylyl cyclase in response to both angiotensin II and vasopressin. The physiological roles of these putative vasopressin receptors are unclear.

Aphasia

The major language centers of the brain. The motor and sensory areas are presented as landmarks. Interconnecting functional pathways are indicated by letters: A) The connection between Wernicke's and Broca's areas, mediating expression of language utterances in speech; B) The connection between Broca's area and the primary motor area; C) Connection between primary auditory perception and Wernicke's area; D) Connection between vision and Wernicke's area, mediating reading ability; E) Connection between somatosensory perception (tactile, pain, cold/hot, position sense) and Wernicke's area, this would mediate language comprehension by tracing letters on the skin or reading braille.

Aphasia: Loss or impairment of language comprehension or production is called aphasia. The difficulties in language function must not be attributable to impairment of the speech or writing production apparatus, such as muscles of the tongue and throat, or peripheral sensory loss. Although the person suffering such impairment may have trouble articulating a language utterance, the brain centers moderating language are presumably intact.

The study of aphasia began with Broca's original case reports of 1861. The first patient could only utter the phrase "tan". Post mortem examination of his brain revealed a fluid filled cavity involving the left frontal lobe. Broca examined another case in which the patient could comprehend but not express language in speech or writing. The patient also had a prominent lesion of the left frontal lobe. In 1865, Broca reported on eight patients who had lost speech and all had left hemisphere lesions.

Broca's reports generated great interest in aphasia and numerous cases were reported that included impairment of the comprehension of language as well as expression. In 1874, Wernicke summarized all these aphasia manifestations and proposed a scheme that included a type of sensory (Wernicke's) aphasia, in which the patient cannot comprehend language and speaks in a fluent, garbled style. This aphasia was caused by lesion of an auditory association area in the superior temporal lobe (Wernicke's area). He also proposed an aphasia syndrome involving the disconnection of the language production centers in the frontal lobe from the comprehension centers in the temporal lobe. This "conduction" aphasia would include an extreme difficulty in repeating language utterances.

The further study of aphasia has essentially followed Wernicke's basic model of analysis. However, numerous subtypes of aphasia have been proposed. Elaborate theories of language function and its mediation by the brain have developed and component language process, such as spelling, writing and reading have been analyzed in detail. Finally, modern neuropsychology includes the study of language mediated by the right hemisphere.

Broca's Aphasia :


Patient's with this form of language disorder cannot fluently express language utterances. Their speech is extremely impoverished or they may be functionally mute. It is not uncommon for their speech to be reduced to a stereotypic nonsense phrase, such as "tan", or "Ichaboty ama". These phrases may be uttered fluently in response to any question, as if they were the remaining language pattern that Broca's area could formulate. Often, phrases such as "yes" and "no", curse words and non language emotional expressions remain intact. Frustrations with language expression often result in curses, or emotionally laden sounds that express frustration. They may also represent the language contribution of the right hemisphere.

Writing is also affected. Although the patients with Broca's aphasia typically have right-sided hemiplegia, their writing disorder extends beyond simple motor incoordination or weakness. Their language production through writing is similar to language production through speech.

In contrast, comprehension of language is relatively intact. The patient understands oral communications from others, and reading may be normal. Although comprehension is invariably superior to expressions, the patient with Broca's aphasia may still have some impairment of comprehension. This distinction involves the contrast between comprehension and expression rather than a complete absence of comprehension deficit.

Patients with Broca's aphasia also have associated findings that aid in clinical diagnosis. First, since the left frontal lobe is involved, they will usually have right-sided hemiplegia. Since most people are left-hemisphere dominant for motor function, damage to motor central areas of the left hemisphere results in extreme motor impairment that compromises the accurate examination of writing abilities. Second, the sensory areas in the posterior parts of the brain are usually intact and it is therefore uncommon for patients with Broca's aphasia to have any sensory deficits. Third, patients with Broca's aphasia often have an apraxia of the left, intact side, that further compromises motor function.

Wernicke's Aphasia :


This aphasia is associated with fluent language output that is severely disorganized, sometimes to the point of an incomprehensible babble. The language constructions are replete with semantic substitutions and paraphasic jargon. Even when the language utterance is grammatically correct, it may be nonsense because of semantic substitution. (e.g., How many sorters were on the wall?).

The other major characteristic is the severe disturbance of comprehension. The patient with Wernicke's aphasia has great difficulty understanding language utterances spoken by others or presented in visual form. This includes their own garbled speech, such that many patients do not understand that their speech is disturbed. Because of this difficulty patients with Wernicke's aphasia have great difficulty repeating phrases presented to them.

They also have trouble in naming objects presented to them. Writing productions have the same quality as speech. Writing samples include nonsense words and semantic substitutions. Reading is severely compromised. The patient often confabulates a reading of text that is garbled nonsense.

Some versions of Wernicke's aphasia include worse visual (reading) than auditory (oral) comprehension. Such patients can understand what others say to them better than comprehending material presented in written form. The opposite pattern is also possible and patients may read better than comprehend oral language. If reading is intact and auditory comprehension is severely impaired then the syndrome is called "pure word deafness". The opposite pattern in which auditory comprehension is intact but reading is impaired is called "pure word blindness".

Wernicke's aphasia results from lesions of the left hemisphere in the region of the auditory association cortex of the superior temporal lobe (Wernicke's area). This area is colored red in the figure above.

Conduction Aphasia :


The comprehension functions of Wernicke's area must interact with the motor and expressive components of Broca's area in order for anyone to engage in meaningful communication. Wernicke proposed the term "conduction aphasia" to describe the language impairment associated with disconnection of these two major language centers. This would involve disconnection of pathway "A" in the figure above.

Patient's with conduction aphasia have fluent paraphasic expression that is characterized by numerous phonetic substitutions (e.g. "fetter" for "better"). Their comprehension is intact. They have a severe impairment of repetition. Reading aloud is characterized by paraphasic output but comprehension is good. Writing impairment is mild.

Lesion of the white matter pathways that connects these areas results in conduction aphasia. The arcuate fasciculus is one the major pathways involved.

Global Aphasia :


This refers to the virtual complete loss of language function as a result of lesion to both Broca's and Wernicke's areas. Surrounding areas of the left hemisphere are usually injured as well. The patient has severe deficits of expression, comprehension, reading, writing, naming, and ability to repeat. Since the left hemisphere is extensively injured, it is possible that the patients remaining language skills represent the language abilities of the right hemisphere.

Transcortical Aphasia - Mixed :


A rare aphasic disorder involves the isolation of both Broca's and Wernicke's areas. The patient has a virtual compulsion to repeat utterances to the point of appearing echolalic. Other language abilities, such as comprehension, naming, expression, and reading are impaired. The patient may not utter any language unless spoken to. Lesion of the "watershed" areas perfused by the middle cerebral artery result in this isolation of the language areas.

Transcortical Aphasia - Motor :


This is a subtype of transcortical aphasia in which motor impairment is greater in comparison to sensory and comprehension impairment. Speech is nonfluent except for repetition. Comprehension is preserved. Reading is consequently intact but writing is impaired. This disorder is similar to Broca's aphasia except for the good ability to repeat. Lesions surrounding Broca's area produce this syndrome.

Transcortical Aphasia - Sensory :


Patients with this subtype of transcortical aphasia have intact repetition and a greater difficulty with comprehension than speech production. Speech is fluent with occasional paraphasic intrusions. The patient appears to have a compulsion to repeat and echo the speech of others. Comprehension is severely limited, resulting in poor reading and writing content. Lesions of sensory association areas surrounding Wernicke's area result in this disorder.


Anomia :

Patients who recover from any form of aphasia often have naming difficulties as a residual symptom. Patients with anomia have a characteristic conversational speech that includes normal fluent output with occasional interruptions as the patient pauses to find the next correct word. These words are invariably names that are not easily retrieved. The patient may also talk around the forgotten word. This feature is called circumlocution. Anomia does not have clear localizing significance. Many lesions of the left hemisphere will produce anomia. Indeed, mild anomia is characteristic of normal language ability. The anomia associated with aphasia appears as a severe form of the word-finding problems that are suffered by everyone.

*Most common language disturbance seen in Head trauma is Anomic Aphasia.
*Most common language disturbance seen in Metabolic encephalopathy is Anomic Aphasia.
*Most common language disturbance seen in Alzheimer's disease is Anomic aphasia.

Aphemia :

This disorder is also called anarthria, subcortical motor aphasia and pure-word dumbness. Patients with this disorder become acutely mute. They recover to have a soft, slow grammatically intact speech. Comprehension, reading and writing are normal. In contrast to pure mutism, they show frustration when unable to speak. Acute lesion of supplementary motor or Broca's areas of the frontal lobe produce this syndrome.

Pure Word Deafness :


This refers to a specific deficit of perception of spoken language. Other auditory perception is intact. Speech is intact but some garbled language may be present at the onset of illness. Writing is normal. Reading may be impaired. Lesion of the primary auditory cortex contiguous to Wernicke's area produces this syndrome.

Alexia :


Alexia without Agraphia (pure alexia)

This disorder involves a disconnection of the language centers from visual perceptual areas. The patient cannot read but other language functions are intact. The patient must have a lesion of the left occipital lobe that also includes the pathways connecting the visual perceptual areas. These pathways make up the splenium of the corpus callosum. This produces a visual field cut on the right side and visual information can only be perceived by the right hemisphere. Since the connections between the right hemisphere visual perception areas and the left hemisphere language centers are lesioned, the patient cannot decode the language related visual information and cannot read. However, the patient comprehends auditory information and can write and speak normally. This results in the paradoxical symptom of a patient who can write spontaneously but cannot read his/her own writing.

Agraphic alexia (Parietal alexia)

This refers to a severe disorder of both reading and writing but auditory comprehension and speech are intact. Acalculia, right-left spatial disorientation and naming deficits are common associated symptoms. Lesions of the left angular gyrus of the parietal lobe result in this syndrome.

Pure Agraphia

This disorder is characterized by agraphia without other language disturbance. Patients make well-formed letters but have characteristic spelling errors. Lesion of the second frontal convolution (Exner's area), superior parietal lobule and perisylvian areas produce this syndrome.

SUMMARY TABLE :

Broca
Nonfluent Speech, Poor Repetition, Good Comprehension, Poor Naming, Right-side Hemiplegia, Few Sensory Deficits

Wernicke
Fluent Speech, Poor Repetition, Poor Comprehension, Poor Naming, No Right-side Hemiplegia, Some Sensory Deficits

Conduction
Fluent Speech, Poor Repetition, Good Comprehension, Poor Naming, No Right-side Hemiplegia, Some Sensory Deficits

Global
Nonfluent Speech, Poor Repetition, Poor Comprehension, Poor Naming, Right-side Hemiplegia, Sensory Deficits

Transcortical Motor
Nonfluent Speech, Good Repetition, Good Comprehension, Poor Naming, Some Right-side Hemiplegia, No Sensory Deficits

Transcortical Sensory
Fluent Speech, Good Repetition, Poor Comprehension, Poor Naming, Some Right-side Hemiplegia, Sensory Deficits

Transcortical Mixed
Nonfluent Speech, Good Repetition, Poor Comprehension, Poor Naming, Some Right-side Hemiplegia, Sensory Deficits

Anomia
Fluent Speech, Good Repetition, Good Comprehension, Poor Naming, No Right-side Hemiplegia, No Sensory Deficit.

Assessment :


Language function is examined using assessment tools designed for two levels of ability: 1) Basic language function, such as simple naming, spelling, repetition and comprehension; 2) Complex language function, such as vocabulary and semantic reasoning. The important constructs to assess in language are spontaneous speech or fluency, naming, repetition, and comprehension. By delineating a profile of performance in each of these areas the clinician can begin to understand the location of the patient's injury and the nature of the language impairment. The following are a selection of language constructs and some assessment strategies:

Spontaneous Speech
This is assessed by requesting the patient to engage in conversation, make social greetings, and describe something, such as a picture. Observations should be made of the patient's speech production. Patients with anterior lesions will have halting, agrammatic, dysprosodic speech which features substantive words, such as the major nouns and verbs. Patients with posterior lesions may speak fluently, with well articulated and prosodic speech, but the speech content will be empty. Paraphasias of semantic or phonemic origin are common.

Repetition
Repetition is assessed by having the patient repeat simple words, and then progressing to more complicated phrases and sentences.

Comprehension
Comprehension is assessed by asking the patient questions which determine accuracy of understanding. This must be distinguished from speech output since many aphasic patients can understand but they cannot indicate their understanding by speaking. Assessment of comprehension includes simple yes/no questions ("do you sit on a chair", "Is your name Joe"), following one step commands ("pick up the keys") and following more complicated two- and three-step commands.

Naming
Naming is assessed by asking the patient to name common objects or pictures of objects. It is important to distinguish between naming impairment, visual/perceptual disturbance, and educational or cultural limitations. Patients should be provided with a descriptive cue ("its something you eat") if they fail to immediately name the object. Also, one cannot assume the patient has a naming deficit if they never knew the name of the object. This can usually be determined by providing a phonemic cue ("the word starts with sphy, for sphynx"). Patients with true naming deficits will usually produce the target word when provided with a phonemic cue, whereas patients who are not familiar with the word will show no response to phonemic cueing.

Factors controlling Insulin secretion

*FACTORS THAT INCREASE INSULIN SECRETION:
- Increase in blood glucose
- Increase in blood free fatty acids
- Increase in blood amino acids
- Gastrointestinal hormones (Gastrin, CCK, Secretin and GIP)
- Glucagon, GH, Cortisol
- Parasympathetic stimulation; Acetyl choline
- Beta-adrenergic stimulation
- Insulin resistance; Obesity
- Sulfonyl urea drugs (Glyburide, Tolbutamide)

*FACTORS THAT DECREASE INSULIN SECRETION:
- Decreased blood glucose
- Fasting
- Somatostatin
- Alpha-adrenergic activity
- Leptin

Skull foramen and structures passing through them

1- HYPOGLOSSAL CANAL - hypoglossal nerve

2- INTERNAL CAROTID ARTERY - passes thru both carotid canal and foramen lacerum

3- GREATER PALATINE FORAMEN - anterior palatine nerve

4- LESSER PALATINE FORAMEN - posterior palatine nerve

5- NASOPALATINE NERVE - incisive foramen

6- SUPRA ORBITAL FORAMEN OR NOTCH - supraorbital nerve

7- SUPRA ORBITAL FISSURE - inferior opthalmic vein

8- INFRA ORBITAL FORAMEN - infra orbital nerve

9- ZYGOMATIC NERVE - infra orbital fissure

10- ZYGOMATICO FACIAL FORAMEN - zygomatico facial branch of the sixth nerve

11- OPTIC CANAL - central retinal vein

12 - FORAMEN ROTUNDUM - maxillary division of the trigeminal nerve

13- FORAMEN OVALE - Mandibular nerve, Accessory meningeal artery, Lesser petrosal nerve and Emissary veins (mnemonic : MALE).

14- FORAMEN SPINOSUM - middle meningeal artery

15- JUGULAR FORAMEN - 9 , 10 , 11 th cranial nerves

16- MASTOID FORAMEN - meningeal branch of occipital artery

17- TYMPANO MASTOID FISSURE - auricular branch of vagus ( vidian r alderman )

18- FACIAL NERVE - stylomastoid foramen

19- CHORDA TYMPANI NERVE - petro tympanic fissure.

Epithelia and their locations in the body

1 - what are the cells that line the alveoli of lungs - simple squamous epithelium

2 - what are the other areas which have the simple squamous epithelium ?

answer : apart from the alveoli of the lungs , it forms the outer capsular wall of renal corpuscles , the thin segments of the renal tubules and various parts of the inner ear .

3- gall bladder epithelium is lined by which epithelium ?

answer : simple columnar epithelium with brush borders .

4- small intestine is lined by which epithelium ?

answer : columnar cells with a striated border of very regular microvilli .

5- respiratory system is mostly lined by which epithelium ?

answer : pseudostratified ciliated columnar epithelium ( upto terminal bronchioles ) .

6- what are the parts of the respiratory system not having the pseudostratified ciliated columnar epithelium ?

answer: alveoli ( simple squamous )

lower pharynx and vocal folds ( oropharynx and laryngopharynx are made up by
the stratified non-keratinised squamous epithelium .)

7 - what are the areas supplied by the stratified keratinised squamous epithelium ?

answer : this type of epithelium is seen in areas which undergo lot of stress and strain and abrasions in addition to exposure to drying . if exposure to drying is absent and there is stress and strain at that region , then a non-keratinised stratified squamous epithelium is seen .
the examples are :

answer----- entire epidermis and mucocutaneous junctions of lips ,
nostrils , distal anal canal ,
outer surface of the tympanic membrane and parts of the oral lining ( gingivae , hard palate and filiform papillae on the anterior surface of the dorsal surface of the tongue .)

8 - what is parakeratinised and orthokeratinised epithelium ?

answer : in some areas of the buccal mucosa , the superficial layers of the otherwise non-keratinised stratified squamous epithelia are partially keratinised giving it the name parakeratinised epithelia . when the keratinisation is full , then it is called orthokeratinised epithelium . ( note : there are areas of the buccal mucosa other than what are mentioned in the question 7 that have non-keratinised stratified squamous epithelium )

9 - what are the regions which have the non-keratinised stratified squamous epithelium ?

answer : other regions of the buccal mucosa other than the regions mentioned in question 7 , part of the anal canal other than the distal part , OROPHARYNX , LARYNGOPHARYNX , OESOPHAGUS , vagina , distal uterine cervix , distal urethra , conjunctiva , cornea and inner surface of the eyelids , the vestibule of the nasal cavities . ( note : the areas which undergo stress and strain and abrasions but are not exposed to drying up or have their own moist system are normally supplied by the non-keratinised stratified squamous epithelium .)

10- and finally where do u see the stratified cuboidal or columnar epithelium ?

answer : in the walls of the larger ducts of some exocrine glands like the pancreas , salivary glands , and the ducts of the sweat glands .

11- stratfied columnar epithelium lines parts of the female urethra ? true or false ?

answer : false . it lines parts of male urethra .

plantar flexion and dorsiflexion - muscles

The principal or main muscles which are responsible for plantar flexion are :

1. gastrocnemius
2. soleus
The prinicipal or main muscles which are responsible for dorsiflexion are :

1. tibialis anterior
( now lets look into the accesory muscles of plantar flexion and dorsiflexion )
The accesory muscles of plantar flexion are :

a. flexor hallucis longus
b. flexor digitorum longus
c. tibialis posterior and
d. plantaris
The accesory muscles of dorsiflexion are :

a. extensor hallucis longus
b. extensor digitorum longus
c. peroneus tertius

Facial nerve subdivisions and functions

Subdivisions and Functions of the Facial Nerve.

Facial Nerve Subdivision	Function
Branchial motor	Muscles of facial expression
	Posterior belly of digastric muscle
	Stylohyoid muscle
	Stapedius muscle
Visceral motor	Salivation—lacrimal, submandibular, and sublingual
	Nasal mucosa or mucous membrane
General sensory	Sensory to auricular concha
	External auditory canal
	Tympanic membrane
Special sensory	Chorda tympani nerve—taste to anterior two-thirds of the tongue

Pneumonia Severity Index (PSI) score or PORT score

*The decision to hospitalize a patient with CAP must take into consideration diminishing health care resources and rising costs of treatment. The cost of inpatient management exceeds that of outpatient treatment by a factor of 20 and accounts for most CAP-related expenditures.

*Certain patients clearly can be managed at home, and others clearly require treatment in the hospital, but the choice is sometimes difficult. Tools that objectively assess the risk of adverse outcomes, including severe illness and death, may minimize unnecessary hospital admissions and help to identify patients who will benefit from hospital care.

*There are currently two sets of criteria: the Pneumonia Severity Index (PSI), a prognostic model used to identify patients at low risk of dying; and the CURB-65 criteria, a severity-of-illness score.

*To determine the PSI, points are given for 20 variables, including age, coexisting illness, and abnormal physical and laboratory findings.

*On the basis of the resulting score, patients are assigned to one of five classes with the following mortality rates:

-class 1, 0.1%;

-class 2, 0.6%;

-class 3, 2.8%;

-class 4, 8.2%; and

-class 5, 29.2%.

*Clinical trials have demonstrated that routine use of the PSI results in lower admission rates for class 1 and class 2 patients. Patients in classes 4 and 5 should be admitted to the hospital, while those in class 3 should ideally be admitted to an observation unit until a further decision can be made.

*The CURB-65 criteria include five variables: 

1. Confusion (C); 

2. Urea >7 mmol/L (U); 

3. Respiratory rate greater than or equal to 30/min (R); 

4. Blood pressure, systolic less than or equal to 90 mmHg or diastolic less than or equal to 60 mmHg (B); and 

5. Age greater than or equal to 65 years (65). 

*Patients with a score of 0, among whom the 30-day mortality rate is 1.5%, can be treated outside the hospital.

*With a score of 2, the 30-day mortality rate is 9.2%, and patients should be admitted to the hospital.

*Among patients with scores of greater than or equal to 3, mortality rates are 22% overall; these patients may require admission to an ICU.

*At present, it is difficult to say which assessment tool is superior. The PSI is less practical in a busy emergency-room setting because of the need to assess 20 variables. While the CURB-65 criteria are easily remembered, they have not been studied as extensively. Whichever system is used, these objective criteria must always be tempered by careful consideration of factors relevant to individual patients, including the ability to comply reliably with an oral antibiotic regimen and the resources available to the patient outside the hospital.

Metabolic syndrome - Clinical identification

Clinical Identification of the Metabolic Syndrome—Any Three Risk Factors

Risk Factor Defining Level Abdominal obesitya   Men (waist circumference)b >102 cm (>40 in.)   Women >88 cm (>35 in.) Triglycerides >1.7 mmol/L (>150 mg/dL) HDL cholesterol   Men <1.0 mmol/L (<40 mg/dL)   Women <1.3 mmol/L (<50 mg/dL) Blood pressure greater than or equal to 130/greater than or equal to 85 mmHg Fasting glucose >6.1 mmol/L (>110 mg/dL)

aOverweight and obesity are associated with insulin resistance and the metabolic syndrome. However, the presence of abdominal obesity is more highly correlated with the metabolic risk factors than is an elevated body-mass index (BMI). Therefore, the simple measure of waist circumference is recommended to identify the BMI component of the metabolic syndrome. bSome male patients can develop multiple metabolic risk factors when the waist circumference is only marginally increased, e.g., 94–102 cm (37–39 in.). Such patients may have a strong genetic contribution to insulin resistance. They should benefit from life-style changes, similarly to men with categorical increases in waist circumference.

Sulci and Gyri of Brain

*Lesion in the broca's area (inferior frontal gyrus) causes broca's aphasia (motor aphasia/expressive aphasia).

*Lesion in the wernicke's aphasia (supramarginal gyrus) of the parietal lobe and upper part of temporal lobe.