The puborectalis muscle, which is one of the muscles that comprise the pelvic floor and plays an important role in both fecal continence and defecation, is tonically contracted and maintains the anorectal angle at rest.

here is a picture: https://www.123rf.com/photo_46940875_stock-vector-the-rectum-and-anus-showing-the-puborectalis-muscle-part-of-the-levator-ani-used-for-the-control-of-.html

I think this is Strongyloides stercoralis (threadworm) is a roundworm whose larvae live in soil and who can cause pulmonary disease. It has the ability to penetrate skin from the soil but can also be obtained by ingesting feces contaminates soil (FA2020 p159) https://www.cdc.gov/parasites/strongyloides/gen_info/faqs.html

Most intestinal roundworms are fecal-oral route except strongyloides which can also penetrate skin, hookworm (necator americanus) which only penetrates skin, and trichinella which can come from undercooked meats (especially pork) but whose symptoms do not match that of the patient. Trichinella larvae enter the blood stream and infect muscle and can also cause trichinosis with fever, nausea, vomiting, periorbital edema, and myalgia.

Grade refers to the differentiation, whereas stage refers to the TNM decriptions

This is high-grade because of the "poorly demarcated... cells growing in sheets" wit a high N:C ratio. Means it's got low differentiation.

This is low-stage because there is NO METASTASIS. Even though there is invasion (and thus, a cancer), M for the TNM is most important.

empty can test isolates the supraspinatus tendon impingement between the acromion and humeral head and finds weakness of the supraspinatus muscle. it is performed by asking the pt. to abduct the arm in the scapular plane at 90 degrees with the arm extended with the the thumb point downwards and asked to abduct the shoulder against resistance. this will reproduced pain and indicate a positive empty can test and indicate supraspinatus tendinopathy

Changes that happen in aging:

Stays the same: TLC (very important to know this)

Increased: lung compliance, residual volume, V/Q mismatch, A-a gradient

Decreased: chest wall compliance, FVC, FEV1, respiratory muscle strength, ventilatory response to hypoxia/hypoxemia

AKA don't get old

UWorld explains it well. Uworld QID: 14781

HLA genes are clustered within a short region of a single chromosome. This results in a low rate of crossover, allowing the HLA gene cluster to be treated as a HLA calotype. Each child inherits 2 halotypes, one from the mother and one from the father. Therefore, the probabilities that a given sibling will share some or all of the same HLA genes are as follows:

• 1/4 chance of inheriting all the same HLA genes (identical match)
• 1/2 chance of inheriting half of the same genes (haploidentical HLA match)
• 1/4 chance of inheriting none of the same HLA genes (HLA mismatch)

Fatty Acid degradation
-Occurs in mitochondria or peroxisomes

First step - uptake of the fatty acids by the cell and addition of CoA to them

Second step - Uptake of the Fatty Acyl CoA molecule into the mitochondria by the Carnitine Shuttle *( which involves removal and then addition of the CoA molecule again to the fatty acid once inside the mitochondria)

Once in the mitochondria the fatty acid may undergo , Beta-oxidation ( a process in which a fatty acid is oxidized/cleaved at the Beta carbon to generate Acetyl CoA in several cycles )

An Acyl CoA dehydrogenase catalyzes the initial step .
Look out for Hypoketotic Hypoglycemia in defects of fatty acid degradation

The 2 main subtypes to be aware of are -a problem with the carnitine shuttle ( systemic carnitine deficiency) - or with an Acyl CoA dehydrogenase ( eg MCAD deficiency )

Fatty Acid degradation
-Occurs in mitochondria or peroxisomes

First step - uptake of the fatty acids by the cell and addition of CoA to them

Second step - Uptake of the Fatty Acyl CoA molecule into the mitochondria by the Carnitine Shuttle *( which involves removal and then addition of the CoA molecule again to the fatty acid once inside the mitochondria)

Once in the mitochondria the fatty acid may undergo , Beta-oxidation ( a process in which a fatty acid is oxidized/cleaved at the Beta carbon to generate Acetyl CoA in several cycles )

An Acyl CoA dehydrogenase catalyzes the initial step .
Look out for Hypoketotic Hypoglycemia in defects of fatty acid degradation

The 2 main subtypes to be aware of are -a problem with the carnitine shuttle ( systemic carnitine deficiency) - or with an Acyl CoA dehydrogenase ( eg MCAD deficiency )

Ugh this question. The Gram stain and purple made me thing Staph aureus, but it also mentions "budding" and "elliptical" (SA is a coccus). Additionally, SA is not a common UTI infection while Candida is.

Annoying because of the Gram stain and purple descriptor.

From quora: "when decolourizer is added, the crystal violet taken up by yeast cells is retained." https://www.quora.com/Why-does-a-yeast-cell-give-Gram-positive-reaction

Fragile X syndrome X-linked dominant inheritance. Trinucleotide repeat in FMR1 gene = hypermethylation = Increased expression.

Most common inherited cause of intellectual disability (Down syndrome is the most common genetic cause, but most cases occur sporadically).

Findings: post-pubertal macroorchidism (enlarged testes), long face with a large jaw, large everted ears, autism, mitral valve prolapse, hypermobile joints.

Trinucleotide repeat expansion [(CGG) n ] occurs during oogenesis.

This patient has pulmonary fibrosis, which causes a restrictive (not obstructive)-type disease. Since there was no occupational exposure, I'm assuming this is idiopathic pulmonary fibrosis. This causes thickened alveolar membranes, limiting gas diffusion. Therefore, eventually O2 won't be able to diffuse quickly enough into the blood across the alveolar-arterial membrane, resulting in a larger A-a difference. (I think there's normally a small A-a gradient, from 2-14 mm Hg, but when this gets too big, you get hypoxic)

ALLELIC HETEROGENEITY (FA page 57 2019)

Theres multiple allele variants for the CFTR gene in a single locus, so you could get cystic fibrosis from a mutation in any one of those allele variants(theres over 1500 different mutations described) the question stem mentioned they tested for the most common types, so we can assume they probably just missed testing for mutations in other alleles.

DOSE x F = AUC x CL

(F= Bioavailability)

If dose is constant and F is increased for Drug X then AUC would increase.

Type I Diabetes is characterized as the destruction of pancreatic islets (specifically beta cells) by T-cells. The most likely cause for hypoglycemia following insulin administration, therefore, is the destruction of alpha cells that surround the beta cells. This would cause decreased levels of circulating glucagon.

Type I Diabetes is characterized as the destruction of pancreatic islets (specifically beta cells) by T-cells. The most likely cause for hypoglycemia following insulin administration, therefore, is the destruction of alpha cells that surround the beta cells. This would cause decreased levels of circulating glucagon.

Type I Diabetes is characterized as the destruction of pancreatic islets (specifically beta cells) by T-cells. The most likely cause for hypoglycemia following insulin administration, therefore, is the destruction of alpha cells that surround the beta cells. This would cause decreased levels of circulating glucagon.