Steroids in asthma facts | Crack PGIMER 22 MAY 2016

Steroids in asthma:

A. Decreases sensitivity of bronchial epithelium to allergen.
B. Decreases inflammatory response.
C. Increases action of bronchodilators. 
D. Cause potent bronchodilation 
E. inhaled corticosteroids have better effectivity than oral doses. 

Answer (A) Decreases sensitivity of bronchial epithelium to allergen

(B) Decreases inflammatory response

• Steroids in asthma reduces bronchial hyperirritability, mucosal oedema and by suppressing inflammatory response to AG : AB reaction or other stimuli.

Steroids are not bonchodilators. 

Selective serotonin Reuptake Inhibitor (SSRI) | Crack PGIMER 22 MAY 2016

Selective serotonin Reuptake Inhibitor (SSRI) are

A. Fluphenazine 
B. Fluoxetine 
C. Fluvoxamine 
D. Sertraline 
E. Fluphenthixol

The Answer is. (B) Fluoxetine;(C) Fluvoxamine;(D) Sertraline

Selective serotonin reuptake inhibitors are

- Fluoxetine

- Fluvoxamine

- Paroxetine

- Sertraline

Fluphenazine, fluphenthixol are antipsychotics (group — phenothiazine, thioxanthine respectively) 

Diarrhoea due to vibrio cholera | Crack PGIMER 22 MAY 2016

In a patient presenting with diarrhoea due to vibrio cholera, which of the following will be present:

A. Abdominal pain 
B. Presence of leukocytes in stool 
C. Fever 
D. Neutrophilia 
E. Ocurrence of many cases in the same locality

The Answer is. (D). Neutrophilia ; (E) Ocurrence of many cases in the same locality

• Vibrio-cholera causes non-inflammatory, painless watery diarrhoea (rice water stool : liquid, turbid, gray cloudy fluid with flakes of mucus and without fecal odour, blood or Pus.) No Fever.

• Mild Neutrophilic Leukocytosis.

• Cholera outbreaks is caused by vibrio choleria-Ol. But the emerging cause of explosive outbreaks is vibrio cholera 0139 Bengal. 

Perforins Production | Crack PGIMER 22 MAY 2016

Perforins are produced by 

A. Cytotoxic T cells 
B. Suppressor T cells 
C. Memory helper T cells 
D. Plasma cells 
E. NK cells

The Answer is. (A) Cytotoxic T cells

• Perforins, are hole forming proteins synthesised by Cytotoxic T-cells.

• Cytotoxic T-cell kill micro-organism, directly attacking cell so called Killer cells. The receptor proteins on surface of cytotoxic cells cause binding tightly to those organism or cells that contain their binding specific antigen. After binding, T cells secrete performs which punch large round holes in the membrane of attacked cell. The released cytotoxins from cytotoxic T-cell attack the cell.

• Suppressor T-cells—suppress the functions of both cytotoxic and helper T-cells. They are responsible for immune tolerance. They are classified as regulatory T-cells.

• The Memory cells are that have ben exposed to antigen and aireadily converted to effector cells by later encounter with the same antige. There is accelerated response to the second exposure. Memory cells are long lived.

• Plasma cells secrete immunoglobulins.

• NK cells Mediate natural immunity, are special population of large lymphocytes, have role in immunity against tumour and transplant cells, mediate action through complements. Cells die of osmotic lysis or apoptosis.

• Granzyme: induces apoptosis in the virus infected cells. Secreated by the cytotoxic T cells

Persistent diarrhoae in AIDS | Crack PGIMER 22 MAY 2016

Persistent diarrhoae in AIDS is caused by all except: 

A. Microspora
B. Cryptosporidium parvum 
C. Cryptococcus 
D. Isospora belli 
E. Giardia lamblia

The Answer is. (C) Cryptococcus ; (E) Giardia lamblia

• Persistent diarrhoea in AIDS is due to infection by

— Cryptosporidia

— Microspora

— Isospora belli

• Cryptococcus causes meningitis, pulmonary infection.

• Giardia lamblia can cause enteric illness with AIDS, neither the course of infection nor the response to the treatment differs from patient with and without AIDS. 

Sterilisation method | Crack AIIMS 8 May 2016 MCQs

Sterilisation method where peritoneum is not entered is:-

A. Vasectomy 
B. Mini lap 
C. Laparoscopy 
D. Transvaginal tubectomy

The Answer is. A. Vasectomy

Vasectomy consists of dividing the vas deferens and disrupting the passage of sperms. It is done through a small incision in the scrotum, under local anaesthesia. 

Traumatic avascular necrosis | Crack PGIMER 22 MAY 2016

Traumatic avascular necrosis occurs in which # 

A. Neck femur 
B. Surgical neck humerus 
C. Talus 
D. Lunate 
E. Scaphoid

The Answer is. (A) Neck femur ; (C) Talus ; (D) Lunate; (E) Scaphod

• Traumatic avascular necrosis is seen with fractures of

— Neck of femur

— Talus

— Scaphoid

— Lunate bone also

• Non-traumatic cases:

• Alcoholism

• Steroid therapy

• Sickle cell disease

• Pt on anticancer drugs, or dialysis

• Postpartum necrosis 

Discrete calcification in Right Hypochondrium | Crack PGIMER 22 MAY 2016

Discrete calcification in right hypochondrium is seen in 

A. Renal calculi 
B. Gall stones 
C. Porcelein gallbladder 
D. Colonic diverticuli
E. Vascular cause

The Answer is. (A) Renal calculi ;(B) Gall stones: (C) Porcelein gallbladder:

Calcification in the right quadrant of the abdomen has several causes. Calcification can be categorized as it can affect the liver, gallbladder, right kidney, digestive tract, peritoneal cavity, right adrenal gland, and retroperitoneum. The Diseases associated with these organs include large gallbladder opaque calculi, echinococcal cysts), schistosomiasis and other granulomatous diseases, calcified renal cysts, renal calculi, calcified nonparasitic liver cysts, primary and metastatic liver tumors, benign liver tumors, and calcification in old adrenal hemorrhage and adrenal masses.

Carcinoembryonic Antigen | Crack PGIMER 22 MAY 2016

True about carcinoembryonic antigen (CEA) 

A. Useful for screening of Ca. colon 
B. gives confirmative evidence of Ca. colon 
C. Helpful for follow-up after resection 
D. Levels decrease immediately after resection of tumor 
E. Tumour mass size correlates with CEA level

The Answer is. (A) Useful for screening of Ca. colon (C) Helpful for follow up after resection (D)Levels decrease immediately after resection of tumor

- CEA is usefull for screening of the some cancers, particularly colon cancer

- CEA is marker to monitor colorectal carcinoma treatment, to identify recurrences after surgical resection, for staging or to localize cancer spread through measurement of biological fluids.

- CEA levels may also be raised in gastric carcinoma, pancreatic carcinoma, lung carcinoma, breast carcinoma, and medullary thyroid carcinoma, as well as some non-neoplastic conditions like ulcerative colitis, pancreatitis, cirrhosis,COPD, Crohn's disease, hypothyroidism.

- It varies inversely with tumor grade (well-differentiated tumors secrete more CEA). CEA is elevated more in tumors with lymph node and distant metastasis than in organ-confined tumors (varies directly with tumor stage). Also, Tumors causing obstruction produce higher CEA levels.

Drug of choice for Methicillin resistant staphylococcus aureus | Crack PGIMER 22 MAY 2016

Drug of choice for Methicillin resistant staphylococcus aureus is (MRSA) 

A. Amoxicillin-Clavulanate
B. Vancomycin 
C. Flucloxacillin 
D. Clindamycin 
E. Erythromycin

The Answer is. (B) Vancomycin

• Vancomycin is the drug of choice of MRSA infections.

• Although sensitive strains may be amenable to therapy with clindamycin or trimethoprimsulfamethoxazole— but many strains are resistant to them.

• New antibiotic quinopristin/dalfopristin and linézolid offer promise for treatment of MRSA, further studies are needed for their recommendation

• Unfortunately, increased use of vancomycin has resulted in emergence of both Vancomycin- Intermediate S. Aureus (VISA), and Vancomycin resistant enterococci (VRE)

• Optimal therapy for VISA is unknown.

Note: Teicoplanin can aiso he used in MRSA infections 

Squamous metaplasia | Crack AIIMS 8 May 2016 MCQs

Squamous metaplasia occurs typically in 

A. bronchi of chronic smokers. 
B. skin exposed to sunlight. 
C. Barrett esophagus. 
D. chronic gastritis.

The answer is A. Long-term smoking irritates the normal columnar bronchial epit helium, which undergoes squamous metaplasia (i.e., it transforms into stratified squamous epithelium). Skin cannot undergo squamous metaplasia, because it is already lined by stratified squamous epithelium. The term callus refers to thickening of the skin it is an example of hyperplasia rather than metaplasia. Barrett’s esophagus represents a form of glandular metaplasia in which the normal squamous epithelium of the esophagus changes into gastric or intestinal epithelium. In chronic gastritis the normal gastric mucosa changes into intestinal epithelium but is not converted into squamous epithelium. 

Sub-epithelial deposits in kidney | Crack PGIMER 22 MAY 2016

Sub-epithelial deposits in kidney are seen in 

A. MPGN-1 
B. GPS (good-pasture syndrome) 
C. PSGN 
D. Membranous UN 
E. RPGN

The Answer is. (A) MPGN-1 ; (C) PSGN; (D) Membranous GN; (E) RPGN: 

Glomerular deposits:

(i), Subepithelial: - Acute GN (like PSGN)

- Membranous GN

- Heyman ON

- RPGN, MPGN (Type-I)

(ii) Sub endothelial

(iii) Basement membrane

- SLE

- Acute GN

- Good pasteure Syndrome

• GPS No deposits, GBM disruptions fibrin are found. 

Conjugated hyperbilirubinemia | Crack PGIMER 22 MAY 2016

Conjugated hyperbilirubinemia in seen in 

A. Rotors synd. 
B. Dubin Johnson syndrome
C. Gilbert’s syndrome
D. Breast milk jaundice 
E. CrigglerNajjar syndrome

The Answer is. A. Rotors synd.

Crigler-Najjar syndrome

There are actually two types of Crigler-Najjar, and both are they different clinically.

Type I CN

-    Rare

-    autosomal recessive disorder

-    Absent UGT1A1 activity. UGT1A1 is a liver enzyme that participates in bilirubin processing

-    The unconjugated bilirubin backs up into the blood, producing severe jaundice and icterus.

-    Usualy fatal in the neonatal period unless liver transplant is done

Type II CN

-    autosomal dominant disorder

-    Some UGT1A1 activity is seen (the enzyme is only capable of forming monoglucuronidated bilirubin).

-    Non fatal, good prognosis.

Gilbert syndrome

-    Common disorder, autosomal recessive

-    Decreased activity of UGT1A1 (but more than Type II Criggler najjar)

-    Unconjugated hyperbilirubinemia, with no clinical consequence

Dubin-Johnson syndrome

-    Autosomal recessive disorder

-    Conjugated bilirubin in the blood.

-    Caused by a defect in secretion of bilirubin glucuronides (which is already conjugated!) across the canalicular membrane (patients are missing a canalicular protein that transports bilirubin glucuronides into bile).

-    Liver biopsy: darkly pigmented because of coarse granules within the hepatocyte cytoplasm.

-    Most patients are asymptomatic (except for yellow skin)

Rotor syndrome

-    Autosomal recessive disorder

-    Conjugated bilirubin in the blood.

-    Unknown defect

-    Asymptomatic (except for mild jaundice)

Must remember:

1.       CD ROM (Conjugated – Dubin, Rotor)   |   Use CNG: (Unconjugated – Criggler Najjar, Gilbert)

All are AR except type II CN

Hypogonadism in cirrhosis caused by | Crack PGIMER 22 MAY 2016

Hypogonadism in cirrhosis is due to 

A. Direct effect of alcohol on testes 
B. Increased estrogen due to decreased catabolism 
C. Increased peripheral conversion of androgens into estrogen 
D. Increased testosterone
E. increased progesterone levels by hepatic hyperactivity

The Answer is. (A) Direct effect of alcohol on testes; (B) Increased estrogen due to decreased catabolism; (C) Increased peripheral conversion of androgens into estrogen

• The testicular atrophy is due to disorder of hormonal metabolism or direct toxic effect on testis.
• In cirrhosis of liver a combined testicular and pituitary abnormality leads to decreased testosterone production. The decreased testo sterone (i.e. androgen insufficiency) production most likely result from inhibition of LH secretion by estrogens in patients with chronic liver disease

• Theincreased estrogen production result from impaired hepatic metabolism and increased extraglandular conversion to estrone and estradiol

Huntington’s disease - hyperkinetic features | Crack AIIMS 8 May 2016 MCQs

In Huntington’s disease, the hyperkinetic features are due to are due to the loss of 

A. Nigrostriatal dopaminergic system
B. Intrastriatal cholinergic system
C. subthalamic neurons
D. Intrastriatal GABA-nergic and cholinergic system

The Answer is. D (Interstitial GABA-nergic and cholinergic system)

Corpus striatum sends inhibitory input to globus pallidus (external); globus pallid us is reciprocally connected with subthalamic nucleus. In Huntington’s disease there is loss of (inhibitory) GABAnergic and cholinergic neurons of the striatum. Loss of inhibition of the external globus pallidus diminishes the activity of neurons in the subthalamic nucleus. Hence, the excitation of neurons of the internal globus pallidus (by subthalamic nucleus) would be reduced. This will inhibit the neurons in the VA and VL nuclei of thalamus. The resulting enhancement of activity of neurons in the cerebral motor cortex may lead to choreiform movements or hyperkinetic features of Huntington’s disease. Loss of dopaminergic neurons in the nigrostriatal tract will lead to Parkinson’s disease. The net effect of such loss/lesion causes an increased activity of neurons in the internal globuspaiidus (a feature opposite to that in Huntington’s disease). This results in greater inhibition of neurons in the VA and VL nuclei of thalamus, and hence less pronounced activation of motor cortex. The consequence is slowed movements (bradykinesia). A lesion of subthalamic nucleus on one side leads to hemiballism: involuntary, violent flailing movements of the limbs on the side opposite to the lesion.

Phantom limb phenomenon | Crack AIIMS 8 May 2016 MCQs

Phantom limb phenomenon can be described by:

A. Weber Fechner law 
B. Power law
C. Bell-Magendie law 
D. Law of projection

The Answer is  ‘D’.  The Law of Projection: “No matter where a particular sensory pathway is stimulated along its course to the cortex, the conscious sensation produced is referred to the location of the receptor.” For example, when the cortical receiving area for impulses from the left hand is stimulated, the patient reports sensation in the left hand, not in the head. Another dramatic example is seen in amputees. Some of these patients may complain, often bitterly, of pain and proprioceptive sensations in the absent limb (phantom limb).

Patient with colon carcinoma metastatic | Crack PGIMER 22 MAY 2016

A 65-year old patient has colon carcinoma metastatic to the liver and lungs. He has weight loss of 10 kg. Cytokine-dependent cachexia is attributable to which of the following

A. Increased glucose uptake and increased glycogen breakdown occurs
B. Suppressed activity of lipoprotein lipase from TNFα
C. TNFα stimulates lipolysis 
D. The differentiation process of pre-adipocyte is impaired 
E. none is true

The Answer Is.: A. Increased glucose uptake and increased glycogen breakdown occurs, B. Suppressed activity of lipoprotein lipase from TNFα , C. TNFa stimulates lipolysis , D. The differentiation process of pre-adipocyte is impaired

Tumor cachexia appears to be mediated via TNFα.

Lipopolysaccharide (LPS), as well as other cytokines, activate a variety of inflammatory cells, importantly macrophages, to produce TNFα.

In vitro, higher TNFα concentrations alter glucose metabolism by increasing glucose uptake and glycogen breakdown and also impairs the Lipogenesis pathway

All of these metabolic effects somewhat explain the chronic syndromes of anorexia, weight loss and cachexia that are associated with chronic infection and malignancy.

TNFα facts | Crack PGIMER 22 MAY 2016

Which of the following statements regarding TNFα are true? 

A. TNFα has a marked procoagulant effect 
B. Passive immunization of patients with neutralizing antibodies to TNFα improves survival from multi-organ system failure 
C. TNFα upregulates P-selectin expression 
D. The most potent known stimulus for TNFα production and release is IL-1
E. all of above

The Answer Is.: A. TNFα has a marked procoagulant effect , C. TNFα upregulates P-selectin expression

Hit points:

ü TNFα has a marked procoagulant effect on endothelial cells, precipitating intravascular thrombosis.

ü TNFα also down regulates the expression of thrombomodulin, which has the potential to block the assembly of protein C and protein S complexes, further decreasing the anticoagulant properties of the endothelial cell surfaces.

ü TNFα upregulates a variety of leukocytic adhesion molecules including ICAM-1, PECAM-1, VCAM-I, F-selectin and P-selectin.

ü A variety of exogenous and endogenous factors (including IL-I) are capable of inducing cells to produce TNFα, however the most potent stimulus for TNFα production and release is endotoxin. 

Cytokines with clearly defined actions in acute inflammation | Crack PGIMER 22 MAY 2016

Cytokines with clearly defined actions in acute inflammation and early tissue injury include which of the following? 

A. Cysteine-X-amino acid Cysteine (CXC) chemokines 
B. Tumor Necrosis Factor (TNF α) 
C. Transforming Growth Factor-beta 
D. Interleukin-1
E. Platelet Derived Growth Factor

The Answer is.: B. Tumor Necrosis Factor (TNF α) , D. Interleukin-1

Polypeptide mediators, such as TNFa and IL-1, are considered “early response” cytokines and are actively involved in the initiation of the cascade of events which precipitate acute inflammation. In addition to being important triggers for the induction of other cytokines important inflammatory network, TNFa and IL-1 appear to be key mediators in promoting the adherence of inflammatory cells to the endothelium. IL-i is a complex, multifunctional molecule that shares many overlapping biological properties with TNFa. In addition, both IL-i and TNFa potentiate the effects of one another. The most important function of 1L-1 appears to be the regulation of the hepatic acute phase response. Following injury, a number of physiologic changes develop within several hours. IL-1 is one of the primary stimuli for the production of acute phase proteins from the liver. Endotoxin, IL-1, TNFa and PDGF are capable of causing significant induction of IL-6 synthesis.

Over the last decade, at least 12 different C-X-C chemokines have been identified. These include IL-8, one of the most potent mediators of chemotaxis known. TNFa and IL-i are key molecules for the induction of IL-8, which in turn is important for the induction of neutrophil recruitment and activation. Similar properties are apparent for other members of this chemokine family.

Platelet activation and degranulation occur during coagulation following injury, leading to the deposition of a number of cytokines into the provisional matrix. These cytokines include transforming growth factor-a, (TGFa), transforming growth factor 3 (TGF-3), platelet- derived growth factor (PDGF), and neutrophil activating peptide-2 (NAP-2). These cytokines are either important growth factors or chemotaxis for leukocytes, endotheIial cells, fibroblasts, and keratinocytes which are key components in the process of tissue repair. Thus, coagulation and platelet activation provide the initial foundation for subsequent cellular recruitment.

Anti diuretic hormone (ADH) | Crack AIIMS 8 May 2016 MCQs

In which of the following forms the Anti diuretic hormone (ADH) is circulated in plasma?

A. Bound to neurophysin – I 
B. Bound to neurophysin – II
C. Bound to plasma albumin 
D. Free from

 The Answer is. B

·   The hormones of the post – pituitary gland (ADH and oxytocin) are synthesized in the cell bodies of magnocellular neurons in the supraoptic and paraventricular nuclei

·   Vasopressin and oxytocin each have a characteristic neurophysin in the granules in the neurons that secrete them. neurophysin II in case of vasopressin and neurophysin I in case of oxytocin.

·   ADH secretion is enhanced by angiotensin II, prostaglandin, histamine, neuropeptide Y and Ach and is inhibited by GABA and ANP.

·   ADH responsive water channel is collecting ducts of kidney is aquaporin – 2 

Patient with Low calcium | Crack AIIMS 8 May 2016 MCQs

A patient is on a Low calcium diet for 6 weeks. He is most likely to have:

A. Raised parathyroid hormone levels
B. Raised calcitonin levels 
C. Increased phosphate levels
D. None of the above

The Answer is A.  Circulating ionized calcium acts directly on the parathyroid glands in a negative feedback fashion to regulate the secretion of PTH. The key to this regulation is a cell membrane Ca₂₊ receptor. This serpentine receptor is coupled via a G protein to phosphoinositide turnover and is found in many tissues. In the parathyroid its its activation inhibits PTH secretion is habited and the Ca₂₊  is deposited in the bones. When it is low, secretion is increased and Ca₂₊  is mobilized from the bones.

Vivo control of citric acid cycle | Crack PGIMER 22 MAY 2016

In vivo control of citric acid cycle is affected by: 

A. Acetyl CoA 
B. Coenzyme A 
C. ATP
D. Citrate
E. NADH

The Answer is. (C) ATP;(E) NADH        

• The citric acid cycle is controlled by regulation of selective enzymes activities — citrate synthase, isocitrate dehydrogenase, c-ketoglutarate dehydrogenase complex.

• Regulation is by availability of ADP

•    ATP, NADH — Inhibitthe cycle

•    Acetyl CO-A formed from pyruvate and CO-A by pyruvatedehydrogenase complex is not a part of TCA cycle.

•    Citrate inhibits phosphofructokinase (Glycolytic enzyme) and activates acetyl co-A carboxylase (Fatty acid synthesis enzyme)

Drugs causing malformation in the fetus | Crack PGIMER 22 MAY 2016

Drugs which cause malformation in the fetus include 

A. Heparin 
B. Warfarin 
C. Valproic acid 
D. Steroids 
E. Phenytoin

The Answer is. (B) Warfarin; (C) Valproic acid; (D) Steroids; (E) Phenytoin

• Heparin doesn’t cross placental barrier.

• Drugs with fetal malformations are:

— Phenytion —* ‘Fetal hydantoin syndrome’ hypoplastic phalanges, cleft lip, cleft palate, microcephaly
— Valproic acid — Neural tube defect, spina bifida

— Warfarin — ‘Chondrodysplasia punctata’ — Craniofacial abnormality

— Steroids — Maternal and Fetal adrenal hypoplasia, cleft palate/lip, cardiac defects 

Skin pigmentation Occurance | Crack PGIMER 22 MAY 2016

Skin pigmentation occurs with which of the following drugs 

A. Clofazimine
B. Minocycline 
C. Sulfonamides 
D. glucosamines 
E. Gold

The Answer is. (A) Clofazimine; (B) Minocycline ;(E) Gold ;

• Pigmentary changes (skin) caused by drugs with their appearance are given below

Note

Appearance — Flat hyperpigmented areas — Blue-black patches — Blue-gray discoloration	Distribution Forehead and cheeks (chloasma, melasma) on shins Light exposed areas	Drugs OCP Minocycline, chloroquine Chiorpromazine and related phenothiazines
— Brown and blue-gray pigmentation Reddish black — Slate-gray colour — Yellow colour	Generalised Sun exposed areas Photo exposed areas	Heavy metals (Ag, Au. Bi, As)ClofazimineAmiodarone

* Chloroquine causes blue-black pigmentation of nails arid palate and depigmentation of hair.

* Zidovudine, hydroxyurea causes brown discolouration of nails.

* Sulphonamidecause fixed drug eruptions.

* Rifampicin cause redish discolouration of sweats.

* Vancomycin causeRedman Syndrome. 

Naltrexone Use in opioid dependence | Crack AIIMS 8 May 2016 MCQs

Naltrexone is used in a case of opioid dependence to 

A. Prevent respiratory depression 
B. To treat withdrawal symptom 
C. To prevent relapse 
D. To treat overdose of opioid

The Answer is. C. (To prevent relapse)

An overdose of opioid can be treated with opioid antagonists (e.g., naloxone and naltrexone). Naltrexone is an orally available opioid antagonist, which block the opioid receptors. When an opioid-dependent person takes opioids, there are no pleasurable experiences. Thus, he does not continue to take opioids, thereby preventing relapse. 

Galactosemia | Crack PGIMER 22 MAY 2016

True regarding galactosemia: 

A. Mental retardation occurs
B. Absent disaccharidase in intestine 
C. Defect in epimerase
D. Defect in galactose 1 P04uridyl transferase 
E. Associated sphingosine receptor defect

The Answer is. (A) Mental retardation occurs; (C) Defect in epimerase (D) Defect in galactose 1 P04 uridyl transferase

• Inability to metabolise Galactose occurs in the Galactosemias which may be caused by deficiency of Galactose-1-phosphate uridyl transferase (Classical Galactosemia), UDP Galactose 4-epimerasè and Galactokinase

• C/F. Jaundice, hepatomegaly, hypoglycemia, vomitting, convulsion, cataract, Mental retardation, vitreous hemorrhage, amino-aciduria, hepatic cirrhosis, ascites, splenomegaly, poor weight-gain, feeding difficulties etc.
• Increased risk for Neonatal Septicemia with E. Coli in galactosemia.